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PubMed1999

Hemodiafiltration for vancomycin overdose in a neonate with end-stage renal failure.

We describe continuous venovenous hemodiafiltration (CVVHD) with a high-flux membrane as a novel treatment modality for vancomycin overdose associated with renal insufficiency. CVVHD was used in a 6-day-old male with a solitary hypodysplastic kidney, suspected sepsis, and anuric renal failure who subsequently received an accidental tenfold overdose of vancomycin. We furthermore present evidence for the importance of countercurrent dialysis in addition to continuous hemofiltration for optimal vancomycin removal.

Drug Overdose↗
PubMed1998

Treatment options for chronic prostatitis due to vancomycin-resistant Enterococcus faecium.

Prostatitis due to vancomycin-resistant enterococci has not been previously described. Reported here is a case of chronic prostatitis due to Enterococcus faecium, resistant to vancomycin, ampicillin, ciprofloxacin and doxycycline, in a 42-year-old liver transplant recipient. Treatment with a combination of rifampin and nitrofurantoin for 6 weeks resulted in long-lasting cure. Other antimicrobial agents active in vitro against vancomycin-resistant enterococci, such as quinupristin/ dalfopristin and chloramphenicol, are unlikely to achieve sufficient prostatic tissue levels to be successfully utilized for treatment of this condition.

Adult↗
PubMed1999

Meropenem alone and in combination with vancomycin in experimental meningitis caused by a penicillin-resistant pneumococcal strain.

In a rabbit model of meningitis caused by a pneumococcus highly resistant to penicillin (MIC, 4 microg/ml), meropenem, a broad-spectrum carbapenem, was bactericidal (-0.48+/-0.14 deltalog10 cfu/ml h) and slightly superior to ceftriaxone (-0.34+/-0.23 deltalog10 cfu/ml x h) and vancomycin (-0.39+/-0.19 deltalog10 cfu/ml x h). Although the combination of vancomycin with ceftriaxone was significantly more active than ceftriaxone alone (-0.55+/-0.19 deltalog10 cfu/ml x h), only an insignificant gain was observed by the addition of vancomycin to meropenem (-0.55+/-0.28 deltalog10 cfu/ml x h).

Animals↗
PubMed2005

Study of the synergism between carbapenems and vancomycin or teicoplanin against MRSA, focusing on S-4661, a carbapenem newly developed in Japan.

S-4661 is a methylcarbapenem antibiotic newly developed in Japan. We evaluated the combined actions of carbapenems, including S-4661 and vancomycin or teicoplanin, against 27 strains of methicillin-resistant Staphylococcus aureus (MRSA) isolated from the blood of patients admitted to Keio University Hospital, using the checkerboard technique. The minimum inhibitory concentrations (MICs) were determined by the Mueller-Hinton agar method. Most of the strains were highly resistant to carbapenems. Synergy with S-4661, panipenem, meropenem or imipenem, and vancomycin was detected against 92% of the strains tested. Synergy with S-4661, panipenem, meropenem or imipenem, and teicoplanin was detected against 74% of the strains tested. The results of our study suggest that combination therapy of vancomycin or teicoplanin with any of S-4661, panipenem, meropenem, or imipenem would be effective for severe infections due to MRSA strains that are resistant to carbapenems.

Anti-Bacterial Agents↗
PubMed1981

Sterilization of Ommaya reservoir by instillation of vancomycin.

We describe the management of a patient with a Staphylococcus epidermidis infection of an Ommaya reservoir that was being used for the treatment of carcinomatous meningitis. Intravenous vancomycin failed to eradicate the organism. We treated our patient successfully with parenteral antibiotics and local instillation of vancomycin (25 micrograms/ml) without removing the reservoir. The patient tolerated the intraventricular vancomycin well. We recommend this approach in the treatment of infected Ommaya reservoirs in patients who have diseases with extremely poor prognoses and who wish to be discharged from the hospital early.

Adult↗
PubMed1983

Efficacy of intravenous vancomycin in the treatment of gram-positive peritonitis in long-term peritoneal dialysis.

Peritonitis is the major complication of long-term peritoneal dialysis. Gram-positive bacteria are responsible for two thirds of the total number of peritonitis episodes. Conventional therapy consists of daily administration of antibiotics, either parenterally or intraperitoneally. Vancomycin, an antibiotic with a prolonged half-life in renal failure, has a wide spectrum of activity against gram-positive bacteria and diffuses readily across the peritoneal membrane. In the present study, 82 percent of gram-positive peritonitis episodes were cured following the intravenous administration of vancomycin at weekly intervals. This cure rate compares favorably with that obtained following conventional therapy of peritonitis. It is concluded that intravenous vancomycin is an effective treatment for gram-positive peritonitis in patients undergoing long-term peritoneal dialysis. This form of therapy is convenient, reduces hospitalization, minimizes cost, and avoids possible contamination of the peritoneal dialysate used during the intraperitoneal administration of antibiotics.

Bacteria↗
PubMed1986

Topical vancomycin formulation for methicillin-resistant Staphylococcus epidermidis blepharoconjunctivitis.

We successfully treated two patients with severe Staphylococcus epidermidis blepharoconjunctivitis by means of a topical vancomycin hydrochloride solution (50 mg/ml) prepared with sterile water. Aqueous vancomycin preparations, however, cause significant ocular irritation probably because of low pH and osmolality values. Solutions prepared with normal saline (5 mg/ml) and phosphate-buffered artificial tears (5 mg/ml and 50 mg/ml) were significantly less irritating and possessed equivalent in vitro antimicrobial activity. Topical vancomycin should be used only when commercially available antibiotics are inadequate.

Administration, Topical↗
PubMed1994

Purification and characterization of the VanB ligase associated with type B vancomycin resistance in Enterococcus faecalis V583.

Acquired resistance to glycopeptides in enterococci is associated with the production of D-Alanine:D-Alanine ligase-related proteins. The VanA protein associated with high-level vancomycin and teicoplanin resistance (VanA phenotype) synthesizes a new peptidoglycan precursor, D-alanine-D-lactate, that has reduced glycopeptide affinity. Production of a similar protein, VanB, is induced in strains that display variable levels of vancomycin resistance but remain susceptible to teicoplanin (VanB phenotype). This paper describes the over-production, purification and characterization of VanB. Comparison of kinetic parameters of the two Van enzymes suggests that differences in catalytic efficiency could account, at least in part, for the various levels of vancomycin resistance.

Amino Acid Sequence↗
PubMed1994

Application of USC*PACK clinical programs to vancomycin in neutropenic patients.

The pharmacokinetics of vancomycin were studied in 10 neutropenic patients (4 male, 6 female) using the USC*PACK Clinical Programs. The experimental data was determined after the first administration of 1000 mg injected as a 1-h infusion. Eight blood samples were collected between 15 min and 11 h after the end of the infusion. Plasma vancomycin concentrations were measured by immunoassay procedure. Creatinine clearance and urine flow were also measured. Pharmacokinetic parameters were computed using a two-compartment model: Vc = 0.270665 +/- 0.161033 (l.kg-1); Kcp = 0.732927 +/- 0.464449 (h-1); Ks = 0.004952 +/- 0.00272 (min.ml-1.h-1); Kpc = 0.470243 +/- 0.194677 (h-1); Ki = 0.011675 +/- 0.004086 (h-1); Ke = 0.644415 +/- 0.239376 (h-1). When we compared this population to the general population of the program, Ke was increased. Elimination constant Ke was not correlated to either creatinine clearance or urine flow. Evaluation of the predictive performance of the Bayesian PC Program for adaptive control of vancomycin therapy in neutropenic patients is the next step of this study.

Adolescent↗
PubMed1993

Emergence of vancomycin-resistant enterococci in New York City.

Enterococci, a common cause of nosocomial infection, are intrinsically resistant to most antimicrobials and readily acquire additional resistance. Vancomycin-resistant enterococci (VRE) have caused clusters of nosocomial infections since 1988. In April, 1991, the New York City Department of Health asked all city laboratories to submit suspected VRE isolates for confirmation. Clinical and epidemiological characteristics of the first 100 patients with VRE were identified, and antimicrobial susceptibility testing, restriction enzyme analysis, and DNA-DNA hybridisation with the vanA gene probe were done. From September, 1989, to October, 1991, 361 patients with VRE were identified at 38 hospitals. The number of hospitals reporting VRE increased from 1 in 1989 to 38 by October, 1991. 98% of 100 VRE infections were nosocomially acquired and 83% patients had received vancomycin and/or a cephalosporin in the 30 days before isolation of VRE. Of 23 isolates from 21 of the first 100 patients, 19 (83%) were resistant to all available antimicrobials. Four vanA probing patterns were noted, and restriction enzyme analysis of the 23 isolates revealed 14 strains. VRE have emerged rapidly in New York City. Molecular analyses suggest that a highly mobile genetic element--eg, a transposon--is responsible for the rapid spread of vancomycin resistance.

Aged↗
PubMed1995

Intracellular activity of both teicoplanin and vancomycin against Staphylococcus aureus in human neutrophils.

The effects in vitro of both teicoplanin and vancomycin of blood peripheral human neutrophils have been studied by assays of antibiotic uptake and intracellular killing of previously phagocytosed Staphylococcus aureus. The effects of vancomycin and teicoplanin (a novel glycopeptide antibiotic), at the therapeutic concentrations reached in plasma (10, 25, 50, 75 and 100 mg/l) and at different times of incubation (5, 15, 30 and 60 min) were studied. The results indicate that: (1) the bactericidal effect of neutrophils increases with incubation time, (2) in the presence of both teicoplanin and vancomycin, the number of CFU/ml of intraphagocytic S. aureus declines with both increasing incubation time and exposure dose of the antibiotics and (3) at 100 mg/l of teicoplanin there is a significant increase in the percentage inhibition of S. aureus growth at all the times studied.

Colony Count, Microbial↗
PubMed1996

In vivo effect of teicoplanin and vancomycin upon haemolytic and bactericidal activity of serum against Staphylococcus aureus.

The present study was undertaken to determine whether teicoplanin and vancomycin influence the hemolytic and bactericidal activity of serum obtained from mice (Swiss, aged 15 +/- 2 weeks). Haemolytic activity was measured in CH-50 units (which represents the capacity of serum complement to lyse 50% of sheep red blood cells in the presence of specific antibody) and the bactericidal activity was estimated from the number of colony-forming units (CFU/ml) of Staphylococcus aureus that survived after 24 h of incubation in the presence of serum. The results indicate that (1) teicoplanin and vancomycin increase the haemolytic activity of serum; (2) in the serum from animals treated with both teicoplanin or vancomycin, the number of CFU/ml of Staphylococcus aureus declines; and (3) these antibiotics appear to have a similar effect upon the complement system.

Animals↗
PubMed1992

Vancomycin-associated linear IgA dermatosis. A report of three cases.

BACKGROUND: Linear IgA dermatosis is an autoantibody-mediated, subepidermal blistering disease that is rarely associated with drug exposure. OBJECTIVE: We report the development of linear IgA dermatosis in three patients associated with the administration of vancomycin and further characterize the immunopathology. METHODS: Direct and indirect immunofluorescence assays were performed to characterize the immunoreactants, determine the subclass of the IgA deposits, and map the site of antibody deposition. RESULTS: A subepidermal blistering disease developed in all patients shortly after vancomycin was initiated, which resolved on discontinuation of the drug. Immunofluorescence studies revealed linear deposits of IgA1 only at the basement membrane zone, below the lamina lucida. Circulating IgA anti-basement membrane zone antibodies were not detected. CONCLUSION: Three patients had linear IgA dermatosis in association with the administration of vancomycin. All patients had linear deposits of IgA1 localized to the sublamina densa zone. Immunophenotypically, the disease in these patients mimics the pattern of IgA deposits seen in the majority of patients with idiopathic linear IgA dermatosis.

Aged↗
PubMed1995

Recommendations for preventing the spread of vancomycin resistance: recommendations of the Hospital Infection Control Practices Advisory Committee (HICPAC).

A rapid increase in the incidence of infection and colonization with vancomycin-resistant enterococci (VRE) has been reported from U.S. hospitals in the last 5 years. This increase poses several problems, including a) the lack of available antimicrobials for therapy of infections due to VRE, since most VRE are also resistant to multiple other drugs, e.g., aminoglycosides and ampicillin, previously used for the treatment of infections due to these organisms, and b) the possibility that the vancomycin resistance genes present in VRE may be transferred to other gram-positive microorganisms such as Staphylococcus aureus. An increased risk of VRE infection and colonization has been associated with previous vancomycin and/or multi-antimicrobial therapy, severe underlying disease or immunosuppression, and intra-abdominal surgery. Because enterococci can be found in the normal gastrointestinal or female genital tract, most enterococcal infections have been attributed to endogenous sources within the individual patient. However, recent reports of outbreaks and endemic infections due to enterococci, including VRE, have shown that patient-to-patient transmission of the microorganisms can occur either via direct contact or indirectly via hands of personnel or contaminated patient-care equipment or environmental surfaces.(ABSTRACT TRUNCATED AT 250 WORDS)

Centers for Disease Control and Prevention, U.S.↗
PubMed1992

Co-transfer of vancomycin and other resistance genes from Enterococcus faecalis NCTC 12201 to Staphylococcus aureus.

Conjugative transfer, in the apparent absence of plasmid DNA, of high-level vancomycin resistance from Enterococcus faecalis NCTC 12201 to Staphylococcus aureus B111 has been demonstrated in vivo and in vitro. Selection of transconjugants on media containing erythromycin or chloramphenicol may result in the transfer of resistance to erythromycin, chloramphenicol, gentamicin, streptomycin and vancomycin though these are capable of separate transfer. Vancomycin resistance has not been transmitted from staphylococcus to staphylococcus though transfer of erythromycin and of chloramphenicol resistance has been achieved.

Conjugation, Genetic↗
PubMed1987

High-performance liquid chromatographic analysis of vancomycin in plasma, bone, atrial appendage tissue and pericardial fluid.

Solid-phase extraction coupled with reversed-phase high-performance liquid chromatography and UV detection was employed for the analysis of the antibiotic vancomycin in patient plasma, bone, atrial appendage, and pericardial fluid. Vancomycin was quantitated in samples from patients undergoing cardiac surgery. Calibrations were linear in the range 3-100 micrograms/ml vancomycin; the lower limit of detection was approximately 3 micrograms/ml in fluids with an absolute limit of detection in bone samples of 0.75 microgram per injection.

Bone and Bones↗
PubMed1986

In vitro evaluation of clindamycin in combination with oxacillin, rifampin, or vancomycin against Staphylococcus aureus.

In a study of antibiotic combinations of clindamycin with rifampin, oxacillin, or vancomycin using the time kill-curve method, the combination of clindamycin and rifampin were sometimes synergistic (5 of 15 times), otherwise indifferent and always enhanced killing of fifteen tested Staphylococcus aureus isolates. In contrast, vancomycin and clindamycin or oxacillin and clindamycin were either indifferent or antagonistic (approximately 50%). Vancomycin alone, however, was generally as effective as the combinations of clindamycin and rifampin.

Clindamycin↗
PubMed1988

Time kill curve analysis of vancomycin and rifampin alone and in combination against nine strains of nutritionally deficient streptococci.

Endocarditis caused by nutritionally deficient streptococci has a high bacteriologic and clinical failure rate, despite appropriate antimicrobial therapy. We investigated by time kill curve methodology nine clinical endocarditis isolates of nutritionally deficient streptococci to determine the in vitro efficacies of vancomycin and rifampin alone and in combination. The combination of vancomycin and rifampin demonstrated synergy and bactericidal activity in five of the strains. In one strain, this combination inhibited growth by greater than 2 log10 CFU/ml when compared to the growth control or either antibiotic alone, but it failed to be bactericidal. Indifference, defined as less than or equal to 2 log10 CFU per milliliter increase in killing of the combination compared to the next most active single agent, was demonstrated with the remaining three isolates. Changing the antibiotic concentrations in the time kill curve studies for these latter strains failed to demonstrate synergistic activity of the antibiotic combination. The vancomycin and rifampin combination may be a promising therapeutic modality for which in vivo correlation is indicated.

Drug Synergism↗