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PubMed2006

Successful therapy of experimental endocarditis caused by vancomycin-resistant Staphylococcus aureus with a combination of vancomycin and beta-lactam antibiotics.

VRS1 is the first isolated strain of vancomycin-resistant Staphylococcus aureus (VRSA) found to carry the vanA gene complex previously described in Enterococcus. Under vancomycin pressure, VRS1 makes aberrant cell walls consisting of stem tetrapeptide and depsipeptide that lack the terminal D-Ala-D-Ala residues targeted by vancomycin. Previous data have suggested that this aberrant cell wall is not cross-linked by PBP2a, the enzyme responsible for cell wall transpeptidation in the presence of beta-lactam antibiotics. We examined the efficacy of treating VRS1 with a combination of vancomycin and beta-lactam antibiotics in vitro and in vivo. We found that the MIC of oxacillin for VRS1 decreased from >256 microg/ml to <1 microg/ml in the presence of vancomycin. Using the rabbit model of endocarditis, we treated VRS1-infected rabbits with nafcillin alone, vancomycin alone, or a combination of nafcillin and vancomycin. Treatment with nafcillin in combination with vancomycin cleared bloodstream infections within 24 h and sterilized 12/13 spleens (92%), as well as 8/13 kidneys (62%), following 3 days of treatment. Mean aortic valve vegetation counts were reduced 3.48 log(10) CFU/g with the combination therapy (compared to untreated controls) and were significantly lower than with either vancomycin or nafcillin given alone. VRS1 was extremely virulent in this model, as no untreated rabbits survived the 3-day trial. Treatment of clinical infections due to VRSA with the combination of vancomycin and beta-lactams may be an option, based on these results.

Animals↗

PubMed1991

Influence of low-level resistance to vancomycin on efficacy of teicoplanin and vancomycin for treatment of experimental endocarditis due to Enterococcus faecium.

Emergence of vancomycin-resistant strains among enterococci raises a new clinical challenge. Rabbits with aortic endocarditis were infected with Enterococcus faecium BM4172, a clinical strain resistant to low levels of vancomycin (MIC, 16 micrograms/ml) and susceptible to teicoplanin (MIC, 1 micrograms/ml), and against its susceptible variant E. faecium BM4172S obtained in vitro by insertional mutagenesis (MICs, 2 and 0.5 micrograms/ml, respectively). Control animals retained 8 to 10.5 log10 CFU/g of vegetation. We evaluated in this model the efficacy of vancomycin (30 mg/kg of body weight; mean peak and trough serum levels, 27 and 5 micrograms/ml, respectively), teicoplanin (standard dose, 10 mg/kg; mean peak and trough levels, 23 and 9 micrograms/ml, respectively; and high dose, 20 mg/kg; mean peak and trough levels, 63 and 25 micrograms/ml, respectively), gentamicin (6 mg/kg; mean peak and trough levels, 8.6 and less than 0.1 micrograms/ml, respectively), alone or in combination, given every 12 h intramuscularly for 5 days. Teicoplanin standard dose was as active as vancomycin against both strains. Vancomycin was not effective against E. faecium BM4172 but was highly effective against E. faecium BM4172S (7.5 +/- 1.1 log10 CFU/g of vegetation versus 4.9 +/- 1.0 log10 CFU/g of vegetation for vancomycin against E. faecium BM4172 and E. faecium BM4172S, respectively; P = 0.0012). A high dose of teicoplanin was more effective than vancomycin against E. faecium BM4172 (4.4 +/- 1.8 log10 CFU/g of vegetation versus 7.5 +/- 1.1 log10 CFU/g of vegetation for teicoplanin high dose and vancomycin, respectively; P less than 0.05). Against E. faecium BM4172 glycopeptide-gentamicin combinations were the most effective regimens in vitro and in vivo (2.8 +/- 0.7 and 3.5 +/- 1.3 log10 CFU/g of vegetation for vancomycin plus gentamicin and teicoplanin standard dose plus gentamicin, respectively; P < 0.05 versus single-drug regimens). We concluded that high-dose teicoplanin or the combination of a glycopeptide antibiotic plus gentamicin was effective against experimental infection due to E. faecium with low-level resistance to vancomycin.

Animals↗

PubMed1999

Combinations of vancomycin and beta-lactams are synergistic against staphylococci with reduced susceptibilities to vancomycin.

Evidence of synergism between combinations of vancomycin and beta-lactam antibiotics against 59 isolates of methicillin-resistant staphylococci (Staphylococcus aureus, Staphylococcus epidermidis, and Staphylococcus haemolyticus) for which vancomycin MICs ranged from 1 to 16 microg/ml were tested by broth microdilution checkerboard, disk diffusion, agar dilution, and time-kill antimicrobial susceptibility tests. The combination of vancomycin and oxacillin demonstrated synergy by all test methods against 30 of 59 isolates; no antagonism was seen. Synergy with vancomycin was also found by modified disk diffusion testing for ceftriaxone, ceftazidime, cefpodoxime, and amoxicillin-clavulanate but not for aztreonam. Evidence of synergy correlated directly with vancomycin MICs. The efficacy of vancomycin given alone and in combination with nafcillin was tested in the rabbit model of experimental endocarditis caused by three clinical isolates of glycopeptide-intermediate-susceptible S. aureus (GISA) (isolates HIP5827, HIP5836, and MU50). Two of the GISA isolates (isolates MU50 and HIP5836) were extremely virulent in this model, with 27 of 42 (64%) animals dying during the 3-day trial. Therapy with either vancomycin or nafcillin given as a single agent was ineffective for animals infected with HIP5827 or MU50. However, the combination of vancomycin and nafcillin resulted in a mean reduction of 4.52 log10 CFU/g of aortic valvular vegetations per g compared to the reduction for controls for animals infected with HIP5827 and a reduction of 4. 15 log10 CFU/g for animals infected with MU50. Renal abscesses caused by HIP5827 were sterilized significantly better with the combination of vancomycin and nafcillin than by either treatment alone. We conclude that the combination of vancomycin and beta-lactams with antistaphylococcal activity is an effective regimen for the treatment of infections with clinical strains of staphylococci which demonstrate reduced susceptibility to glycopeptides.

Animals↗

PubMed2003

Vancomycin treatment failure associated with heterogeneous vancomycin-intermediate Staphylococcus aureus in a patient with endocarditis and in the rabbit model of endocarditis.

Heterogeneous resistance to vancomycin is thought to precede emergence of intermediate susceptibility to vancomycin in Staphylococcus aureus, but the clinical significance of heterogeneous resistance is unknown. Paired S. aureus isolates from a patient with endocarditis who relapsed after vancomycin treatment were tested for heterogeneous resistance to vancomycin. The pretreatment and the relapse clinical isolates (strains SF1 and SF2, respectively) were genotyped by pulsed-field gel electrophoresis. Susceptibility to vancomycin was assessed by the broth dilution method, population analysis, and time-kill studies and in the rabbit model of endocarditis. Strains SF1 and SF2 had similar genotypes, and the vancomycin MICs for the strains were </=2 micro g/ml. SF2 exhibited heterogeneous resistance to vancomycin. Vancomycin eradicated SF1 in the rabbit model of endocarditis, while SF2 persisted at pretreatment levels. Vancomycin treatment failure in this patient with endocarditis was attributable to heterogeneous resistance to vancomycin.

Animals↗

PubMed1995

Vancomycin-dependent Enterococcus faecium isolated from stool following oral vancomycin therapy.

The isolation of clinical strains of enterococci requiring vancomycin for growth has only recently been reported. We describe the isolation of Enterococcus faecium requiring vancomycin for growth from the stool of a patient who had completed oral vancomycin therapy. Growth of the vancomycin-dependent E. faecium was supported by ristocetin and D-alanyl-D-alanine but not by daptomycin, teicoplanin, or D,L-alanine. Spontaneous revertants not requiring vancomycin occurred at a rate of 1 in 10(6). Both the vancomycin-dependent E. faecium and the revertant hybridized with a vanB gene probe and had identical contour-clamped homogeneous electrophoresis patterns. The majority of revertant colonies were resistant to teicoplanin, suggesting constitutive production of the vanB ligase. We believe the vancomycin-dependent E. faecium evolved from a vancomycin-resistant, vancomycin-independent E. faecium in the presence of high concentrations of vancomycin in the intestine.

Aged↗

PubMed1999

The association between antecedent vancomycin treatment and hospital-acquired vancomycin-resistant enterococci: a meta-analysis.

BACKGROUND: The association between vancomycin hydrochloride treatment and vancomycin-resistant enterococci (VRE) has been investigated in numerous studies with variable results. OBJECTIVES: To conduct a meta-analysis to estimate the magnitude of the association between vancomycin treatment and individual risk of VRE and to identify study characteristics that accounted for heterogeneity in study results. METHODS: Studies were identified using MEDLINE with index terms "Enterococcus," "Enterococcus faecalis," or "Enterococcus faecium" and "vancomycin," "drug resistance," "drug resistance, microbial," or "drug resistance, multiple or risk factors." Reports from conferences and reference lists of recent reviews were used. A total of 420 published reports and 98 conference reports were reviewed; 20 studies described in 15 published reports were included in the analysis. We recorded study period, hospital setting, case and control definitions, length of hospital stay, method of adjustment for differences in length of stay, and data on treatment with vancomycin. The odds ratio (OR) of vancomycin treatment provided the measure of association analyzed. A random-effects model was used to estimate the pooled OR. RESULTS: When results from all 20 studies were combined, the pooled OR was 4.5 (95% confidence interval, 3.0-6.9), but the test for heterogeneity was highly significant (P<.001). The 5 studies that used patients with vancomycin-susceptible enterococci as controls found a stronger association (pooled OR, 10.7; 95% confidence interval, 4.8-23.8) than the 15 studies that used controls who had no VRE isolated (pooled OR, 2.7; 95% confidence interval, 2.0-3.8). After restricting the analysis to the latter studies only, no heterogeneity was evident in the unadjusted study results. Patients with VRE had stayed in the hospital much longer than control patients. Studies that adjusted for this difference found only a small and nonsignificant association between vancomycin treatment and VRE (pooled OR, 1.4; 95% confidence interval, 0.74-2.60). We also detected publication bias, favoring report of studies that found a large measure of association. CONCLUSIONS: The reported strong association between vancomycin treatment and hospital-acquired VRE results from the selection of the reference group, confounding by duration of hospitalization, and publication bias. Studies that accounted for these factors found only a small and nonsignificant association.

Adult↗

PubMed2002

Emergence of vancomycin resistance during therapy against methicillin-resistant Staphylococcus aureus in a burn patient--importance of low-level resistance to vancomycin.

OBJECTIVES: Staphylococcus aureus with low-level resistance to vancomycin (VLSA) which could develop into vancomycin-resistant S. aureus (VRSA) is most important. However, VLSA is difficult to detect by standard laboratory methods. We describe here improved methods to detect VLSA. METHODS: Three methicillin-resistant S. aureus (MRSA) strains, designated Fu6, Fu10, and Fu18, were sequentially isolated from the burn wound site of a patient, during vancomycin therapy. The properties of these strains were compared with those of reference strains Mu3 and Mu50 (previous resistant isolates from other patients). RESULTS: The isolated strains, Fu10 and Fu18, had identical phenotypes and genotypes. The vancomycin resistance of Fu10 was equivalent to that of strain Mu3, whereas Fu18 had much higher vancomycin resistance than Fu10 and Mu3, although reaching the level of Mu50. Fu18 showed similar growth to Mu50 on gradient gels and on Mu3 medium. CONCLUSIONS: Our data indicate that the VLSA developed vancomycin resistance during exposure to vancomycin in vivo. The population analysis of tested VLSA and vancomycin intermediately resistant S. aureus (VISA) indicates that a penem at relatively low concentrations induced a significant increase in the number of vancomycin-resistant subpopulations. Furthermore, we confirmed that gradient gel analysis and Mu3 medium are simple and useful methods for the detection of VLSA judged as VSSA by its conventional MIC alone.

Anti-Bacterial Agents↗

PubMed1998

Third-generation cephalosporins and vancomycin as risk factors for postoperative vancomycin-resistant enterococcus infection.

OBJECTIVE: To examine use of third-generation cephalosporins (3GCs) alone and in association with vancomycin hydrochloride as a risk factor for vancomycin-resistant enterococcus (VRE) infection in surgical patients. DESIGN: Case-control retrospective study analyzing antibiotic use in the 30 days preceding culture of VRE or vancomycin-sensitive enterococcus from an infected site. SETTING: A large tertiary care teaching hospital. PATIENTS: Surgical inpatients with VRE infections between September 3, 1993, and January 29, 1997, were matched with patients with vancomycin-sensitive enterococcus infections. Matches were based on surgical procedure, initial infection site, and immunosuppression. Matches were found for 32 of 50 surgical patients with VRE. Twenty matched pairs of patients were recipients of solid organ transplants. MAIN OUTCOME MEASURES: Multivariate logistic regression analysis was done to examine 3GCs and vancomycin as risk factors for VRE infection. Univariate analysis of use of other antibiotic agents and demographic data was also performed. RESULTS: Multivariate analysis showed significant differences in the use of 3GCs both alone and concurrently with vancomycin. Univariate analysis also showed higher use of metronidazole, concurrent vancomycin and metronidazole, concurrent vancomycin and ceftazidime, and all antibiotics combined in patients with VRE infections. CONCLUSIONS: This matched control study showed that use of 3GCs, alone (P=.05) or concurrently with vancomycin (P=.05), was a risk factor for VRE infection in surgical patients. Judicious administration of third-generation antibiotics is warranted in surgical patients with other risk factors for VRE.

Adult↗

PubMed1996

Limiting vancomycin use to combat vancomycin-resistant Enterococcus faecium.

The implementation, monitoring, and impact of a program to restrict vancomycin use are described. A vancomycin restriction program was implemented in February 1995 at an acute care teaching hospital after guidelines for vancomycin use were established by a multidisciplinary group. Pharmacists reviewed each vancomycin order, suggested alternative treatments when vancomycin use did not comply with the guidelines, and set duration limits for all orders. Orders requiring greater clinical experience for review were referred to a pharmacist or a physician in the division of infectious diseases. The program was monitored by an infectious diseases pharmacist. Data collected after the program was established showed that the volume of vancomycin use decreased substantially. Problems in enforcing the restriction program included administration of vancomycin for surgical prophylaxis before the order reached the pharmacy, continuing use of vancomycin for initial empirical treatment of febrile neutropenic and immunocompromised patients, inadequate tracking of the evaluations, and deficiencies in the evaluations related to a need for continuing education of the pharmacists about the program. Use of vancomycin decreased after a pharmacy-enforced restriction program was implemented.

Anti-Bacterial Agents↗

PubMed1993

Vancomycin binding to cell walls of non-streptococcal vancomycin-resistant bacteria.

The availability of peptidoglycan for binding to vancomycin was investigated in intrinsically vancomycin-resistant clinical isolates of Leuconostoc mesenteroides, Lactobacillus viridescens and Pediococcus pentosaceus. Intrinsic vancomycin resistance expressed by L. mesenteroides and P. pentosaceus was the result of poor binding of vancomycin to native or SDS-treated cell walls. Pre-exposure of L. viridescens to vancomycin decreased the subsequent binding of vancomycin to the cell walls, suggesting an alternative mechanism to that found in high-level vancomycin-resistant enterococci and intrinsically-resistant L. mesenteroides and P. pentosaceus. Vancomycin binding was sensitive to substitution of larger side chains at the C-terminus. Variations of peptidoglycan peptide types found in L. mesenteroides, L. viridescens and P. pentosaceus could account for their intrinsic vancomycin resistance.

Amino Acid Sequence↗

PubMed2001

Bacteriocin production in vancomycin-resistant and vancomycin-susceptible Enterococcus isolates of different origins.

Bacteriocin production was determined for 218 Enterococcus isolates (Enterococcus faecalis [93] and E. faecium [125]) obtained from different origins (human clinical samples [87], human fecal samples [78], sewage [28], and chicken samples [25]) and showing different vancomycin susceptibility patterns (vancomycin resistant, all of them vanA positive [56], and vancomycin susceptible [162]). All enterococcal isolates were randomly selected except for the vancomycin-resistant ones. A total of 33 isolates of eight different bacterial genera were used as indicators for bacteriocin production. Forty-seven percent of the analyzed enterococcal isolates were bacteriocin producers (80.6% of E. faecalis and 21.6% of E. faecium isolates). The percentage of bacteriocin producers was higher among human clinical isolates (63.2%, 81.8% of vancomycin-resistant isolates and 60.5% of vancomycin-susceptible ones) than among isolates from the other origins (28 to 39.3%). Only one out of the 15 vancomycin-resistant isolates from human fecal samples was a bacteriocin producer, while 44.4% of fecal vancomycin-susceptible isolates were. The bacteriocin produced by the vanA-containing E. faecium strain RC714, named bacteriocin RC714, was further characterized. This bacteriocin activity was cotransferred together with the vanA genetic determinant to E. faecalis strain JH2-2. Bacteriocin RC714 was purified to homogeneity and its primary structure was determined by amino acid sequencing, showing an identity of 88% and a similarity of 92% with the previously described bacteriocin 31 from E. faecalis YI717. The presence of five different amino acids in bacteriocin RC714 suggest that this could be a new bacteriocin. The results obtained suggest that the epidemiology of vancomycin resistance may be influenced by different factors, including bacteriocin production.

Amino Acid Sequence↗

PubMed1997

Effect of a vancomycin restriction policy on ordering practices during an outbreak of vancomycin-resistant Enterococcus faecium.

BACKGROUND: With the development of nosocomial pathogens that are resistant to multiple antimicrobial agents, reasonable restriction of antibiotic use has become a priority. METHODS: During an outbreak of vancomycin-resistant enterococcal infections, an audit of vancomycin hydrochloride use was conducted during October 3 through 21, 1994, and January 24 through February 2, 1995. During these periods, all orders for vancomycin were reviewed by clinical pharmacists. Use was classified as either appropriate or inappropriate based on recommendations by the Hospital Infection Control Practice Advisory Committee (HICPAC) of the Centers for Disease Control and Prevention, Atlanta, Ga. A policy restricting the use of vancomycin was adopted in November 1994. RESULTS: During the first audit in October 1994, 61% of vancomycin orders were considered inappropriate according to HICPAC criteria. At the time of this audit, the first cases of an outbreak of nosocomial vancomycin-resistant Enterococcus faecium had been detected. The follow-up audit showed that 30% of vancomycin orders were inappropriate by HICPAC criteria (P < .001). Overall use of vancomycin decreased by 50% and remained at this lower level for the following year. CONCLUSION: The institution of a vancomycin restriction policy was associated with a reduction of both inappropriate drug orders and total use.

Anti-Bacterial Agents↗

PubMed2002

Effectiveness of a multifaceted infection control policy in reducing vancomycin usage and vancomycin-resistant enterococci at a tertiary care cancer centre.

We undertook a prospective cohort study to evaluate the role of a multifaceted infection control policy including the use of a "vancomycin order form," in decreasing the transmission of vancomycin-resistant enterococci (VRE). In January 1997, a multifaceted infection-control policy was implemented amongst patients admitted to the M. D. Anderson Cancer Center in whom neutropenic fever developed or who were found to be colonized or infected with VRE. As part of this programme, we initiated the use of a vancomycin order form to reduce the use of empirical vancomycin. The total incidence of VRE infections declined from 0.437/1000 patient days in 1996-97 to 0.229/1000 patient days in 1998-99 (P=0.008). The VRE bloodstream infections declined from 0.338/1000 patient days in 1996-97 to 0.181/1000 patient days in 1998-99 (P=0.027). Empiric vancomycin use decreased from 416 g/1000 patient days in 1996-97 to 208 g/1000 patient days in 1998-99 (P<0.001), resulting in a decreased vancomycin cost from $2561 US dollars/1000 patient days in 1996-97 to $1195 US dollars/1000 patient days in 1997-98 (P<0.001). We conclude that a multifaceted infection control policy incorporating the use of a vancomycin order form can effectively decrease the use of empirical vancomycin and can play a role in limiting the spread of VRE in an endemic setting.

Anti-Bacterial Agents↗

PubMed2004

Vancomycin-resistant Staphylococcus aureus in the absence of vancomycin exposure.

We report findings from our investigation of the world's second clinical isolate of vancomycin-resistant Staphylococcus aureus (VRSA). An elderly man was hospitalized with an infected chronic heel ulcer and osteomyelitis. Before hospital admission, he received multiple courses of antibiotic therapy but, notably, no vancomycin. Numerous cultures of ulcer specimens (performed on an outpatient basis) grew methicillin-resistant, vancomycin-susceptible S. aureus and vancomycin-resistant Enterococcus species. At admission, an additional culture of a specimen from the heel ulcer grew S. aureus that was identified as VRSA (minimal inhibitory concentration for vancomycin [by broth-microdilution], 32 microg/mL). Further evaluation confirmed the presence of the vanA gene mediating vancomycin resistance. To assess VRSA transmission, we performed a carriage study of 283 identified contacts and an environmental survey of the patient's home; no VRSA isolates were recovered. This case illustrates that recent exposure by patients to vancomycin is not necessary for development of vanA-containing VRSA. For clinical and public health reasons, it is essential that microbiology laboratories adequately test for vancomycin-resistance in S. aureus.

Aged↗

PubMedDate not supplied

Structure-binding relationships for the interaction between a vancomycin monoclonal antibody Fab fragment and a library of vancomycin analogues and tracers.

A series of vancomycin analogues and tracers were synthesized, and their binding interactions with an anti-vancomycin Fab fragment were evaluated under mass transport limiting conditions using surface plasmon resonance detection. Differences observed in binding interactions were utilized to define the vancomycin structural elements critical for antibody recognition. Major structural regions of vancomycin shown to play an important role in anti-vancomycin Fab fragment recognition include two sugar moieties and one chlorinated phenyl ring. The N-methylleucyl residue, the carboxy terminal residue, and residues in the peptide-binding region of vancomycin have minimal impact on the anti-vancomycin Fab fragment/vancomycin binding interaction. The selection of an antibody with such binding properties plays a critical role in the development of a vancomycin immunoassay that employs stable calibrators and controls.

Antibodies, Monoclonal↗

PubMed2001

Outpatient vancomycin use and vancomycin-resistant enterococcal colonization in maintenance dialysis patients.

BACKGROUND: Although outpatient vancomycin is widely used as empiric therapy for dialysis-associated infections, its relationship with vancomycin-resistant enterococcal (VRE) colonization is not established. METHODS: During a two-year prospective cohort study, rectal swabs obtained from patients at the start and finish of the study period and during interim hospitalizations were cultured for VRE. RESULTS: Ten of 124 patients initially grew VRE. Twenty-four of the remaining patients had no follow-up cultures because of patient death (62%), transfer to another dialysis facility (17%), patient's refusal (7%), and transplantation (4%), and were thus excluded. The remaining patients (N = 90) had a median age of 54.3 years and were 92% African American and 50% male. Fifty-eight percent were treated by hemodialysis. They received 403 g of intravenous vancomycin over 157.2 patient-years of follow-up, 73% as outpatients. Sixteen of 90 patients (17.8%) became colonized with VRE, an incidence rate of one case per 9.8 patient-years of follow-up. None of the 29 patients who did not receive vancomycin developed VRE compared with 26% of those treated with vancomycin (P = 0.001). The odds ratio (95% CI) for the association of outpatient vancomycin (g per year) with VRE colonization was 1.23 (1.05, 1.44, P = 0.008). The association remained significant following adjustment in separate logistic regression analyses for relevant demographic, clinical, antimicrobial (inpatient vancomycin, oral or intravenous cephalosprins, aminoglycosides, quinalones, or antianaerobics), and hospitalization exposures. The unadjusted relative risk of death in patients growing VRE was significantly higher than in those not colonized with VRE (P = 0.005). CONCLUSIONS: VRE colonization is a relatively common and under recognized problem among chronic dialysis patients. It is strongly and independently associated with the outpatient use of vancomycin, which should be avoided whenever possible.

Adult↗

PubMed1995

Vancomycin or vancomycin plus netilmicin for methicillin- and gentamicin-resistant Staphylococcus aureus aortic valve experimental endocarditis.

Using a rabbit model of aortic valve endocarditis, we studied the efficacy of vancomycin alone or in combination with netilmicin and/or rifampin against a methicillin- and gentamicin-resistant strain of Staphylococcus aureus (MGRSA). Antibiotics were given for 6 to 12 days, as follows: vancomycin (15 mg/kg of body weight every 12 h [BID] intravenously), vancomycin plus netilmicin (2.5 mg/kg BID intramuscularly), vancomycin plus rifampin (10 mg/kg BID intramuscularly), and vancomycin plus netilmicin plus rifampin at the same routes, dosages, and schedules mentioned above. Netilmicin was given to two additional groups at a higher dosage (6 mg/kg every 24 h intramuscularly) alone or in combination with vancomycin (15 mg/kg BID intravenously) for 12 days. All regimens resulted in undetectable bacterial counts in a significant proportion of vegetations (except netilmicin alone) or reduced the bacterial counts in the vegetations compared with the counts in the untreated controls (P<0.01 to P<0.001). No resistance to rifampin or netilmicin developed during therapy. It is concluded that in the treatment of experimental aortic valve endocarditis caused by MGRSA (i) vancomycin as monotherapy is as efficacious as the triple combination, (ii) the addition of netilmicin (once daily or BID) to vancomycin does not improve the efficacy of the latter antibiotic, even in the presence of rifampin, and (iii) a 12-day course in more effective than a 6-day one, but not at a statistically significant level.

Animals↗

PubMed1998

Successful vancomycin desensitization in a patient with end-stage renal disease and anaphylactic shock to vancomycin.

OBJECTIVE: To report successful desensitization in a patient with a history of end-stage renal disease (ESRD) and anaphylactic shock after receiving vancomycin. CASE SUMMARY: A 47-year-old white woman with a history of ESRD was admitted to the hospital reporting persistent nausea, vomiting, and diffuse abdominal pain. She had developed anaphylactic shock after exposure to vancomycin 3 years prior to this hospitalization. The patient's hospital course was complicated by septic shock and positive blood cultures for methicillin-resistant Staphylococcus epidermidis. The patient tolerated vancomycin desensitization and received intravenous vancomycin 100 mg/d for 21 days. DISCUSSION: The desensitization protocol used in this report allows for gradual increases in vancomycin serum concentrations, avoiding peak and trough concentrations that occur with intravenous boluses. Maintaining the desensitized state is dependent on the continuous presence of the antigen with a return of clinical sensitivity after drug discontinuation. The vancomycin desensitization protocol and subsequent dosing strategy was used to ensure the continuous presence of vancomycin at steady-state concentrations to prevent the return of anaphylactic sensitivity. CONCLUSIONS: Desensitization was successful in a patient with ESRD and history of anaphylactic shock to vancomycin.

Anaphylaxis↗