PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Vancomycin Resistance”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed2003

In vitro antimicrobial activity of linezolid tested against vancomycin-resistant enterococci isolated in Brazilian hospitals.

The emergence of vancomycin-resistant enterococci (VRE) has been described recently in Brazil. This is in contrast to the USA and Europe, where the VRE appeared in the late 1980s. The progressive increase in VRE isolation poses important problems in the antimicrobial therapy of nosocomial infections. Treatment options and effective antimicrobial agents for VRE are often limited and the possibility of transfer of vancomycin genes to other Gram-positive microorganisms continues. In the search for antimicrobial agents for multiresistant Gram-positive cocci, compounds such as linezolid and quinupristin/dalfopristin have been evaluated. The present study was conducted to evaluate the in vitro activity of the oxazolidinone linezolid and 10 other antimicrobial agents, including quinupristin-dalfopristin, against multiresistant enterococci isolated in Brazilian hospitals. Thirty-three vancomycin resistant isolates (17 Enterococcus faecium and 16 E. faecalis), were analyzed. Strains were isolated from patients at São Paulo Hospital, Oswaldo Cruz Hospital, Hospital do Servidor Público Estadual, Santa Marcelina Hospital, Santa Casa de Misericórdia de São Paulo, and Hospital de Clínicas do Paraná. The samples were tested by a broth microdilution method following the National Committee for Clinical Laboratory Standards (NCCLS) recommendations. All isolates were molecular typed using pulsed-field gel electrophoresis (PFGE). Linezolid was the most active compound against these multiresistant enterococci, showing 100% inhibition at the susceptible breakpoints. Quinupristin/dalfopristin and teicoplanin showed poor activity against both species. The molecular typing results suggest that there has been interhospital spread of vancomycin resistant E. faecium and E. faecalis among Brazilian hospitals. The results of this study indicate that linezolid is an appropriate therapeutic option for the treatment of vancomycin-resistant enterococci infections in Brazil.

Acetamides↗
PubMed2005

[Incidence of vancomycin-resistant Enterococcus at a university hospital in Brazil].

OBJECTIVE: Vancomycin-resistant Enterococcus (VRE) is today one of the principal microorganisms implicated in nosocomial infections. Thus, a study was carried out with the objective of evaluating its epidemiology at a tertiary-level teaching hospital. METHODS: This was a three-year retrospective epidemiological study conducted from 2000 to 2002. Samples of VRE-positive clinical cultures at a 660-bed university hospital were analyzed. The incidence of VRE and the main anatomical sites and hospital units from which it was isolated were defined. Differences between the variables over the three years of the study were verified, and these were considered significant when p<0.05. RESULTS: There was a progressive increase in the vancomycin resistance in the clinical cultures that were positive for Enterococcus spp., over the three years of the study. In 2000, 9.5% of the samples were vancomycin-resistant, and this increased to 14.7% in 2001 and 15.8% in 2002. The hospital units with the largest numbers of isolates were, respectively, the emergency ward (19.5%) and the general intensive care unit (15%). The anatomical sites with the highest amounts of isolates included: urine (36%) and blood (20%). CONCLUSIONS: With the progressive increase in the incidence of vancomycin resistance and the VRE rate, it is concluded that more effective control measures are needed for deterring the dissemination of VRE.

Brazil↗
PubMed1996

Treatment of vancomycin-resistant staphylococcal infections.

The reports of vancomycin resistance, though sparse, cannot be ignored. They document evidence of emerging vancomycin resistance. Because of the absence of suitable alternatives and a poor current understanding of the mechanisms involved, much work is needed to prevent such resistance from becoming widespread. Only by understanding the mechanism(s) of resistance involved can we develop strategies to combat resistant strains.

Adult↗
PubMed1997

Are clinical laboratories in California accurately reporting vancomycin-resistant enterococci?

In order to determine whether hospital-based clinical laboratories conducting active surveillance for vancomycin-resistant enterococci in three San Francisco Bay area counties (San Francisco, Alameda, and Contra Costa counties) were accurately reporting vancomycin resistance, five vancomycin-resistant enterococcal strains and one vancomycin-susceptible beta-lactamase-producing enterococcus were sent to 31 of 32 (97%) laboratories conducting surveillance. Each strain was tested by the laboratory's routine antimicrobial susceptibility testing method. An Enterococcus faecium strain with high-level resistance to vancomycin (MIC, 512 microg/ml) was correctly reported as resistant by 100% of laboratories; an E. faecium strain with moderate-level resistance (MIC, 64 microg/ml) was correctly reported as resistant by 91% of laboratories; two Enterococcus faecalis strains with low-level resistance (MICs, 32 microg/ml) were correctly reported as resistant by 97 and 56% of laboratories, respectively. An Enterococcus gallinarum strain with intrinsic low-level resistance (MIC, 8 microg/ml) was correctly reported as intermediate by 50% of laboratories. A beta-lactamase-producing E. faecalis isolate was correctly identified as susceptible to vancomycin by 100% of laboratories and as resistant to penicillin and ampicillin by 68 and 44% of laboratories, respectively; all 23 (74%) laboratories that tested for beta-lactamase recognized that it was a beta-lactamase producer. This survey indicated that for clinically significant enterococcal isolates, laboratories in the San Francisco Bay area have problems in detecting low- to moderate-level but not high-level vancomycin resistance. Increasing accuracy of detection and prompt reporting of these isolates and investigation of cases are the next steps in the battle for control of the spread of vancomycin resistance.

Ampicillin↗
PubMed2000

Vancomycin resistance and antibiotic susceptibility of enterococci in raw meat.

The purpose of this study was to investigate antimicrobial resistance, in particular to vancomycin, of enterococci in samples (100) of meat (beef, chicken, turkey, lamb, and pork) sold in retail outlets of Catanzaro (Italy). Enterococci were identified to the species level. Antimicrobial susceptibility tests for a large spectrum of antibiotics including glycopeptides were performed by the disk diffusion method. Kappa statistic was used to evaluate associations of resistance to vancomycin with other antimicrobials. Enterococci were isolated from 45% of the samples, mostly from chicken meat (65.4%). Overall, 29% of samples were contaminated by vancomycin-resistant enterococci (VRE), whereas among those positive they represented 64.4% of isolates. Higher prevalence of vancomycin resistance was found in chicken samples (76.5%). The overall resistance to teicoplanin (TRE) was 30%, whereas among those positive, TRE represented 66.7% of isolates. The most frequent isolates were Enterococcus faecium (35.6%) and Enterococcus faecalis (33.3%). Resistance to vancomycin and teicoplanin was observed in 75% and 78.5% of E. faecium, and in 40% and 46.7% of E. faecalis, respectively. Most strains were susceptible to ampicillin (80%), while 88.9% were resistant to methicillin. The most effective antimicrobials were imipenem (73.3% susceptible) and rifampin (80%). The highest prevalence of resistance was for streptomycin (88.9%), tetracycline (84.4%), and erythromycin (75.6%). Resistance to vancomycin was significantly associated to methicillin, teicoplanin, erythromycin, tetracycline, and chloramphenicol. Further investigations about enterococcal colonization and infections in community and hospital subjects are needed.

Animals↗
PubMed2000

Mechanism-based inactivation of VanX, a D-alanyl-D-alanine dipeptidase necessary for vancomycin resistance.

VanX is a zinc-dependent D-Ala-D-Ala amino dipeptidase required for high-level resistance to vancomycin. The enzyme is also able to process dipeptides with bulky C-terminal amino acids [Wu, Z., Wright, G. D., and Walsh, C. T. (1995) Biochemistry 34, 2455-2463]. We took advantage of this observation to design and synthesize the dipeptide-like D-Ala-D-Gly(SPhip-CHF(2))-OH (7) as a potential mechanism-based inhibitor. VanX-mediated peptide cleavage generates a highly reactive 4-thioquinone fluoromethide which is able to covalently react with enzyme nucleophilic residues, resulting in irreversible inhibition. Inhibition of VanX by 7 was time-dependent (K(irr) = 30+/-1 microM; k(inact) = 7.3+/- 0.3 min(-1)) and active site-directed, as deduced from substrate protection experiments. Nucleophilic compounds such as sodium azide, potassium cyanide, and glutathione did not protect the enzyme from inhibition, indicating that the generated nucleophile inactivates VanX before leaving the active site. The failure to reactivate the dead enzyme by gel filtration or pH modification confirmed the covalent nature of the reaction that leads to inactivation. Inactivation was associated with the elimination of fluoride ion as deduced from (19)F NMR spectroscopy analysis and with the production of fluorinated thiophenol dimer 12. These data are consistent with suicide inactivation of VanX by dipeptide 7. The small size of the VanX active site and the presence of a number of nucleophilic side chains at the opening of the active site gorge [Bussiere, D. E., et al. (1998) Mol. Cell 2, 75-84] associated with the high observed partition ratio of 7500+/-500 suggest that the inhibitor is likely to react at the entrance of the active site cavity.

Bacterial Proteins↗
PubMed2002

Biochemical and genetic characterization of the vanC-2 vancomycin resistance gene cluster of Enterococcus casseliflavus ATCC 25788.

The vanC-2 cluster of Enterococcus casseliflavus ATCC 25788 consisted of five genes (vanC-2, vanXY(C-2), vanT(C-2), vanR(C-2), and vanS(C-2)) and shared the same organization as the vanC cluster of E. gallinarum BM4174. The proteins encoded by these genes displayed a high degree of amino acid identity to the proteins encoded within the vanC gene cluster. The putative D,D-dipeptidase-D,D-carboxypeptidase, VanXY(C-2), exhibited 81% amino acid identity to VanXY(C), and VanT(C-2) displayed 65% amino acid identity to the serine racemase, VanT. VanR(C-2) and VanS(C-2) displayed high degrees of identity to VanR(C) and VanS(C), respectively, and contained the conserved residues identified as important to their function as a response regulator and histidine kinase, respectively. Resistance to vancomycin was expressed inducibly in E. casseliflavus ATCC 25788 and required an extended period of induction. Analysis of peptidoglycan precursors revealed that UDP-N-acetylmuramyl-L-Ala-delta-D-Glu-L-Lys-D-Ala-D-Ser could not be detected until several hours after the addition of vancomycin, and its appearance coincided with the resumption of growth. The introduction of additional copies of the vanT(C-2) gene, encoding a putative serine racemase, and the presence of supplementary D-serine in the growth medium both significantly reduced the period before growth resumed after addition of vancomycin. This suggested that the availability of D-serine plays an important role in the induction process.

Bacterial Proteins↗
PubMed2001

Bacteremic infection with Pediococcus: vancomycin-resistant opportunist.

Pediococci are recently recognized Gram-positive human pathogens, resistant to vancomycin and generally susceptible to penicillin. Infection in adults has been seen in patients with chronic underlying conditions as well as those with previous abdominal surgery. Two previous infants with congenital gastrointestinal malformations requiring surgical correction have been reported with sepsis attributable to Pediococcus sp. We report a third infant born with gastroschisis who developed Pediococcus bacteremia and meningitis 3 months after surgery, and speculate regarding the role of probiotics in the pathogenesis of this infection.

Bacteremia↗
PubMed2002

A PCR assay for rapid detection of vancomycin-resistant enterococci.

Since the first report of a vancomycin-resistant enterococcal clinical isolate, these Gram-positive bacteria have emerged as important nosocomial pathogens. Several glycopeptide resistance phenotypes can be distinguished on the basis of the level and inducibility of resistance to vancomycin and teicoplanin. In the present study, we developed a multiplex PCR, which allows the simultaneous identification of enterococci at the genus level and detection of the most frequent glycopeptide resistance genotypes. Five primer sets targeting the genes vanA, vanB, vanC1, vanC2/C3 and tuf were used in one reaction tube with bacterial DNA extracted from three to five colonies. This PCR method is suitable for the rapid detection of vancomycin-resistant enterococci.

DNA, Bacterial↗
PubMed1995

Vancomycin-resistant Enterococcus faecium sepsis following persistent colonization.

Vancomycin-resistant enterococci have emerged as important nosocomial pathogens and represent a serious threat to patients with impaired host defenses. We describe a patient with leukemia who developed prolonged colonization with vancomycin-resistant Enterococcus faecium and ultimately died of sepsis due to this multidrug-resistant organism. This case report confirms that colonization with vancomycin-resistant enterococci may last indefinitely and that asymptomatic carriage can lead to invasive infection.

Adult↗
PubMed1988

Vancomycin-resistant gram-positive bacteria isolated from human sources.

Recent reports of infections with vancomycin-resistant gram-positive bacteria prompted us to study vancomycin-resistant isolates from human sources to characterize the types of bacteria displaying this phenotype. Thirty-six vancomycin-resistant gram-positive isolates, 14 from clinical specimens and 22 from stool samples, were identified. These isolates were tentatively identified as Lactobacillus spp. (25 strains), Leuconostoc spp. (6 strains), and Pediococcus spp. (3 strains) on the basis of morphology and physiological tests. Two isolates of indeterminate morphology could not be unambiguously assigned to a genus. Four isolates of vancomycin-resistant lactobacilli from normally sterile body sites were considered to be clinically significant. Vancomycin-resistant gram-positive bacteria may represent an emerging class of nosocomial pathogens. Better methods for distinguishing the various genera in the clinical microbiology laboratory are needed.

Adult↗
PubMed1995

Recommendations for preventing the spread of vancomycin resistance.

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 multiantimicrobial 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. Prevention and control of the spread of vancomycin resistance will require coordinated, concerted effort from various departments of the hospital, and can only be achieved if each of the following elements is addressed: 1) prudent vancomycin use by clinicians, 2) education of hospital staff regarding the problem of vancomycin resistance, 3) early detection and prompt reporting of vancomycin resistance in enterococci and other gram-positive microorganisms by the hospital microbiology laboratory, and 4) immediate implementation of appropriate infection-control measures to prevent person-to-person transmission of VRE.

Cross Infection↗
PubMed1996

Semisynthetic glycopeptide antibiotics derived from LY264826 active against vancomycin-resistant enterococci.

Certain derivatives of the glycopeptide antibiotic LY264826 with N-alkyl-linked substitutions on the epivancosamine sugar are active against glycopeptide-resistant enterococci. Six compounds representing our most active series were evaluated for activity against antibiotic-resistant, gram-positive pathogens. For Enterococcus faecium and E. faecalis resistant to both vancomycin and teicoplanin, the MICs of the six semisynthetic compounds for 90% of the strains tested were 1 to 4 micrograms/ml, compared with 2,048 micrograms/ml for vancomycin and 256 micrograms/ml for LY264826. For E. faecium and E. faecalis resistant to vancomycin but not teicoplanin, the MICs were 0.016 to 1 micrograms/ml, compared with 64 to 1,024 micrograms/ml for vancomycin. The compounds were highly active against vancomycin-susceptible enterococci and against E. gallinarum and E. casseliflavus and showed some activity against isolates of highly vancomycin-resistant leuconostocs and pediococci. The MICs for 90% of the strains of methicillin-resistant Staphylococcus aureus tested were typically 0.25 to 1 micrograms/ml, compared with 1 microgram/ml for vancomycin. Against methicillin-resistant S. epidermidis MICs ranged from 0.25 to 2 micrograms/ml, compared with 1 to 4 micrograms/ml for vancomycin and 4 to 16 micrograms/ml for teicoplanin. The spectrum of these new compounds included activity against teicoplanin-resistant, coagulase-negative staphylococci. The compounds exhibited exceptional potency against pathogenic streptococci, with MICs of < or = 0.008 microgram/ml against Streptococcus pneumoniae, including penicillin-resistant isolates. In in vivo studies with a mouse infection model, the median effective doses against a challenge by S. aureus, S. pneumoniae, or S. pyogenes were typically 4 to 20 times lower than those of vancomycin. Overall, these new glycopeptides, such as LY307599 and LY333328, show promise for use as agents against resistant enterococci, methicillin-resistant S. aureus, and penicillin-resistant pneumococci.

Animals↗
PubMed2006

Pheromone-responsive conjugative vancomycin resistance plasmids in Enterococcus faecalis isolates from humans and chicken feces.

The drug resistances and plasmid contents of a total of 85 vancomycin-resistant enterococcus (VRE) strains that had been isolated in Korea were examined. Fifty-four of the strains originated from samples of chicken feces, and 31 were isolated from hospital patients in Korea. Enterococcus faecalis KV1 and KV2, which had been isolated from a patient and a sample of chicken feces, respectively, were found to carry the plasmids pSL1 and pSL2, respectively. The plasmids transferred resistances to vancomycin, gentamicin, kanamycin, streptomycin, and erythromycin to E. faecalis strains at a high frequency of about 10(-3) per donor cell during 4 hours of broth mating. E. faecalis strains containing each of the pSL plasmids formed clumps after 2 hours of incubation in broth containing E. faecalis FA2-2 culture filtrate (i.e., the E. faecalis sex pheromone), and the plasmid subsequently transferred to the recipient strain in a 10-min short mating in broth, indicating that the plasmids are responsive to E. faecalis pheromones. The pSL plasmids did not respond to any of synthetic pheromones for the previously characterized plasmids. The pheromone specific for pSL plasmids has been designated cSL1. Southern hybridization analysis showed that specific FspI fragments from each of the pSL plasmids hybridized with the aggregation substance gene (asa1) of the pheromone-responsive plasmid pAD1, indicating that the plasmids had a gene homologous to asa1. The restriction maps of the plasmids were identical, and the size of the plasmids was estimated to be 128.1 kb. The plasmids carried five drug resistance determinants for vanA, ermB, aph(3'), aph(6'), and aac(6')/aph(2'), which encode resistance to vancomycin, erythromycin, kanamycin, streptomycin, and gentamicin/kanamycin, respectively. Nucleotide sequence analyses of the drug resistance determinants and their flanking regions are described in this report. The results described provide evidence for the exchange of genetic information between human and animal (chicken) VRE reservoirs and suggest the potential for horizontal transmission of multiple drug resistance, including vancomycin resistance, between farm animals and humans via a pheromone-responsive conjugative plasmid.

Animals↗
PubMed2006

Detection of heterogeneous, intermediate-vancomycin-resistant Staphylococcus aureus (hVISA) using low-concentration vancomycin disks.

Heterogeneous, intermediate-vancomycin-resistant Staphylococcus aureus (hVISA) represents a threat of an incurable infection since the first report in 1997. The method used to detect hVISA isolates is a population analysis profile (PAP); however, it is impractical for routine laboratory analysis. We therefore tested a simple, reliable and inexpensive method for the detection of hVISA. Eighteen isolates of hVISA and 22 of vancomycin-sensitive S. aureus (VSSA) were included. The organisms were tested by the disk diffusion method, using 15-microg vancomycin disks on four different media: Mueller-Hinton agar (MHA), MHA plus 2% NaCI (MHAS), Brain Heart Infusion agar (BHA), and BHA plus 2% NaCl (BHAS). In addition, two different inoculum sizes, bacterial suspensions adjusted to 0.5 and 2.0 McFarland, were tested. The inhibition zone was read independently by three medical technologists after incubation at 37 degrees C for 24 and 48 hours. The use of MHAS with an inoculum size of 2.0 McFarland and 48-hour incubation period yielded the highest sensitivity (94.4%), specificity (81.8%), positive predictive value (80.9%), and negative predictive value (94.7%). The disk diffusion test with 15-microg vancomycin disk is simple and may be used as a screening method for the detection of hVISA.

Culture Media↗
PubMed1999

Antimicrobial susceptibilities of clinical isolates of vancomycin-resistant enterococci in Taiwan.

To understand the antimicrobial resistance patterns of vancomycin-resistant enterococci in Taiwan, we tested the in vitro activities of 10 antimicrobial agents against 71 clinical isolates (39 of Enterococcus faecalis and 32 of Enterococcus faecium) by means of the agar dilution method. Resistance was determined on the basis of the minimum inhibitory concentration (MIC) of each antimicrobial agent--MIC50 and MIC90 (minimum concentrations required to inhibit growth of 50% and 90% of isolates, respectively) were determined. No beta-lactamase producers were identified with the cefinase test. All E. faecalis isolates were susceptible to penicillin and ampicillin, and 97% of these isolates were resistant to teicoplanin (vanA phenotype). Of the E. faecium isolates, 75% were susceptible to teicoplanin (vanB phenotype) and most were resistant to penicillin (94%) and ampicillin (94%). Quinupristin/dalfopristin was markedly less active against E. faecalis than E. faecium isolates (MIC50, 64 vs 2 micrograms/mL; MIC90, 128 vs 8 micrograms/mL; susceptibility rates, 3% vs 81%). Five of the eight vanA phenotype E. faecium isolates and one of the 24 vanB phenotype E. faecium isolates were resistant to quinupristin/dalfopristin. The activity of rifampin was also species-specific, with E. faecium being markedly less susceptible to this agent than E. faecalis (MIC50, 16 vs 1 microgram/mL; MIC90, 64 vs 4 micrograms/mL). Our data suggest the potential of teicoplanin and quinupristin/dalfopristin as appropriate antimicrobial agents in the treatment of infections caused by vanB phenotype E. faecium. Penicillin, ampicillin, and rifampin alone, or preferably in combination with other agents, appear to be the most appropriate agents for the treatment of vancomycin-resistant E. faecalis infections in Taiwan.

Drug Resistance, Microbial↗
PubMed1998

Antibiotic resistance patterns of enterococci and occurrence of vancomycin-resistant enterococci in raw minced beef and pork in Germany.

The food chain, especially raw minced meat, is thought to be responsible for an increase in the incidence of vancomycin-resistant enterococci (VRE) in human nosocomial infections. Therefore, 555 samples from 115 batches of minced beef and pork from a European Union-licensed meat-processing plant were screened for the occurrence of VRE. The processed meat came from 45 different slaughterhouses in Germany. Enterococci were isolated directly from Enterococcosel selective agar plates and also from Enterococcosel selective agar plates supplemented with 32 mg of vancomycin per liter. In addition, peptone broth was used in a preenrichment procedure, and samples were subsequently plated onto Enterococcosel agar containing vancomycin. To determine resistance, 209 isolates from 275 samples were tested with the glycopeptides vancomycin, teicoplanin, and avoparcin and 19 other antimicrobial substances by using a broth microdilution test. When the direct method was used, VRE were found in 3 of 555 samples (0.5%) at a concentration of 1.0 log CFU/g of minced meat. When the preenrichment procedure was used, 8% of the samples were VRE positive. Our findings indicate that there is a low incidence of VRE in minced meat in Germany. In addition, the resistance patterns of the VRE isolates obtained were different from the resistance patterns of clinical isolates. A connection between the occurrence of VRE in minced meat and nosocomial infections could not be demonstrated on the basis of our findings.

Animals↗