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PubMed1997

In vitro activity of chloramphenicol alone and in combination with vancomycin, ampicillin, or RP 59500 (quinupristin/dalfopristin) against vancomycin-resistant enterococci.

Using a checkerboard assay, ampicillin, vancomycin, and RP 59500, each in combination with chloramphenicol, were tested for synergy against 23 isolates of vancomycin-resistant enterococci. Additive effects were seen in 62.5% of the isolates when exposed to chloramphenicol plus RP 59500. Additive effects were observed in 20% and 15% of isolates with chloramphenicol plus vancomycin or ampicillin, respectively. No antagonism was noted.

Ampicillin↗
PubMed1998

In vitro susceptibility and molecular analysis of gentamicin-resistant enterococci.

Enterococci with gentamicin MICs of 256 to 1,024 micrograms/mL were evaluated for susceptibility to ampicillin plus gentamicin synergism. Sixteen of eighteen enterococcal isolates were not susceptible to synergistic killing by ampicillin plus gentamicin; 11 possessed aac(6')-aph(2"), and 4 possessed aph(2")-Ic. A gentamicin MIC of 512 or 1,024 micrograms/mL predicted lack of ampicillin/gentamicin synergism, but a gentamicin MIC of 256 micrograms/mL did not. For six enterococcal strains possessing the gentamicin-resistance gene aph(2")-Ic, ampicillin plus dibekacin, ampicillin plus netilmicin, and ampicillin plus amikacin produced synergistic killing in five, three, and two strains, respectively.

Amikacin↗
PubMed1998

In vitro activity of RPR 106972 alone and in combination with vancomycin, ampicillin, and gentamicin against multidrug-resistant enterococci.

This investigation used checkerboard and time-kill assays to evaluate the in vitro activity of RPR 106972 (45% pristinamycin IB and 55% pristinamycin IIB) alone and in combination with vancomycin or ampicillin +/- gentamicin against multidrug-resistant enterococci. The checkerboard procedure resulted in synergistic or additive effects in 91% of the isolates with the combination of RPR 106972 plus vancomycin versus 68% with RPR 106972 plus ampicillin. The addition of gentamicin to either combination resulted in synergistic or additive results in 100% of the isolates. Inhibitory activity was observed with the time-kill assay with mean change in log10 CFU/mL at 24 h of -0.31 for RPR 106972, 3.3 for vancomycin, -0.46 for RPR 106972 plus vancomycin, and -0.35 for RPR 106972 plus vancomycin and gentamicin. No antagonism was noted with any of the combinations. RPR 106972 demonstrates good inhibitory activity against Enterococcus faecium and may prove useful in the treatment of enterococcal infections.

Ampicillin↗
PubMed1999

Vancomycin-resistant enterococci: the clinical effect of a common nosocomial pathogen.

Enterococcus spp. is now the third most common pathogen among hospitalized patients, accounting for nearly 12% of nosocomial infections. Enterococcus faecalis is the most prevalent enterococcal species (85%-89%), whereas Enterococcus faecium accounts for 10%-15% of enterococcal isolates. Only 5% of E. faecalis isolates are resistant to glycopeptides. E. faecium has also been shown to be resistant to nonglycopeptide compounds, such as penicillins (97%), high-level gentamicin (52.1%), and high-level streptomycin (58.3%). Numerous risk factors for vancomycin-resistant enterococci (VRE) have been identified, including as length of hospital- or ICU-stay, proximity to a hospitalized, colonized VRE, patient severity of illness, renal failure, recent surgery, immunosuppression, and organ recipient status. An important risk factor is prior exposure to antibiotics such as vancomycin, ceftazidime, ciprofloxacin, and metronidazole, as well as the number and duration of recent antibiotics. Interventions to reduce nosocomial VRE cross-transmission have also been studied. Using gowns in addition to gloves diminished the incidence of VRE in one study, but had a negligible effect in a second study. Studies have shown that in many cases (> 60%) vancomycin usage is inappropriate. While controlling the use of vancomycin alone has only variably diminished VRE colonization, other efforts such as narrowing the spectrum of antibiotics, antiseptics, and reducing immunosuppression may be salutary. Attempts to eradicate VRE intestinal carriage with enteral agents (bacitracin, tetracycline + rifampin, novobiocin) have been reported but seem to have only a transient effect. Non-antimicrobial interventions such as removal of intravenous or bladder catheters and/or surgical or percutaneous drainage may be beneficial. In addition, the development of new antimicrobial agents such as streptogramins, glycopeptides, everninomicins, and oxazalididones will hopefully play an important role in reducing morbidity from these pathogens.

Anti-Bacterial Agents↗
PubMed1999

Synergistic effect of gentamicin plus ampicillin on enterococci with differing sensitivity to gentamicin: a phenotypic assessment of NCCLS guidelines.

Between December 1, 1993, and December 1, 1996, we tested 4,411 isolates of Enterococcus sp. at gentamicin concentrations of 500 micrograms/mL and 2000 micrograms/mL using agar dilution to phenotypically categorize them into 3 groups: those with a MIC < or = 500 micrograms/mL (n = 3,132; 71%); a MIC > 500, but < or = 2000 micrograms/mL (n = 441; 10%); and those with a MIC > 2000 micrograms/mL (n = 838; 19%). Ten unique strains of each phenotype were tested to determine which gentamicin concentration was the best in vitro predictor of synergy with ampicillin. Testing was done by a time-kill method using clinically achievable levels of ampicillin and gentamicin. We found that for the gentamicin MIC < or = 500 micrograms/mL group, 7 of 10 isolates demonstrated synergy with ampicillin as manifested by a > or = 2 log10 increase in killing versus the effect of ampicillin alone (at 1/2 the MIC for ampicillin). In the group sensitive to a gentamicin MIC range between > 500 and < or = 2,000 micrograms/mL, none of the 10 isolates demonstrated synergy. Absence of synergy was also found in the group resistant to 2,000 micrograms/mL of gentamicin. Assessment of eight additional enterococcal isolates with reduced sensitivity to ampicillin (MIC from 32-256 micrograms/mL) found no correlation between gentamicin sensitivity at 500 micrograms/mL and any in vitro test for synergy, nor with clinical therapeutic outcome. Gentamicin at 2 micrograms/mL combined with ampicillin was as effective in enhancing killing as a higher level of 4 micrograms/mL. These findings validate the current NCCLS guideline for predicting synergistic activity against enterococci in strains with usual susceptibility to ampicillin, and suggest that a therapeutic level less than maximal recommended dosing is sufficient when using gentamicin in this setting.

Ampicillin↗
PubMed1997

Vancomycin-resistant enterococci. Mechanism and clinical relevance.

Vancomycin-resistant enterococci have spread widely throughout the United States. Mechanisms of glycopeptide resistance are understood to a significant extent. These organisms are associated with considerable morbidity. Treatment options are limited, and control of their spread requires considerable effort and results in increased costs.

Anti-Bacterial Agents↗
PubMed2001

Lactoferrin-induced reduction of vanB vancomycin resistance in enterococci.

The mucosal protein lactoferrin (LF) reduces the MIC of vancomycin for staphylococcal isolates sensitive to this glycopeptide. The purpose of this research was to investigate the effect of LF on the MIC of vancomycin for vanB resistant isolates of Enterococcus faecalis (Efs1) and E. faecium (Efm1). At a concentration of 2048 microg/ml, LF reduced the MIC of vancomycin 16-fold for Efs1 and eight-fold for Efm1. The cell wall precursors of Efs1 were examined following growth in media supplemented with LF, D-alanine or D-lactate. The precursors were extracted from harvested cells by ether and ion exchange chromatography and the amino acid and lactate composition was determined. Compared with that of unsupplemented media, D-alanine or LF supplementation caused an increase in the D-alanine content of the precursors. Concomitantly, the D-lactate content was reduced. Exogenous D-lactate did not affect the composition of the precursors. This suggests that LF caused an increase in the pool of pentapeptide cell wall precursors. The LF-induced reduction in the vancomycin resistance of enterococci at in vivo concentrations suggests a potential use for this protein as an adjunctive agent to vancomycin.

Cell Wall↗
PubMed1999

In vitro selection of glycopeptide-resistant variants of Enterococci.

In order to study the possible phenotypic and genotypic changes related to glycopeptide pressure on enterococci, a study was undertaken using stepwise in vitro exposure to achieve the following objectives: (i) to evaluate the development of resistance and cross-resistance between vancomycin and teicoplanin; (ii) to determine the stability of the acquired level of resistance; (iii) to determine the phenotypic and genotypic changes related to glycopeptide pressure; and (iv) to assess the spectrum of antibiotic-susceptibility of all strains. Our results showed that no variants resistant to glycopeptides could be selected after in vitro glycopeptide exposure experiments. However some strains showed increased MIC values: 8 mg/l to vancomycin in eight strains selected by vancomycin itself, while teicoplanin produced intermediate values to vancomycin in only three strains. The phenotypes were stable in vitro after numerous passages in antibiotic-free medium and three out of nine strains with a changed MIC level, showed 40, 42 and 43 kDa proteins in cell membrane preparations. The profile of antibiotic resistance was comparable in all isogenic strains tested with the exception of three selected strains that became susceptible to penicillin G. The pressure produced by glycopeptides, particularly vancomycin has contributed to an increased level of MIC that can influence the acquisition and/or full expression of this resistance.

Anti-Bacterial Agents↗
PubMed2000

Vancomycin resistance in enterococci: reprogramming of the D-ala-D-Ala ligases in bacterial peptidoglycan biosynthesis.

Vancomycin binds to bacterial cell-wall intermediates to achieve its antibiotic effect. Infections of vancomycin-resistant enterococci are, however, becoming an increasing problem; the bacteria are resistant because they synthesize different cell-wall intermediates. The enzymes involved in cell-wall biosynthesis, therefore, are potential targets for combating this resistance. Recent biochemical and crystallographic results are providing mechanistic and structural details about some of these targets.

Enterococcus↗
PubMed1999

Prodigious substrate specificity of AAC(6')-APH(2"), an aminoglycoside antibiotic resistance determinant in enterococci and staphylococci.

BACKGROUND: High-level gentamicin resistance in enterococci and staphylococci is conferred by AAC(6')-APH(2"), an enzyme with 6'-N-acetyltransferase and 2"-O-phosphotransferase activities. The presence of this enzyme in pathogenic gram-positive bacteria prevents the successful use of gentamicin C and most other aminoglycosides as therapeutic agents. RESULTS: In an effort to understand the mechanism of aminoglycoside modification, we expressed AAC(6')-APH(2") in Bacillus subtilis. The purified enzyme is monomeric with a molecular mass of 57 kDa and displays both the expected aminoglycoside N-acetyltransferase and O-phosphotransferase activities. Structure-function analysis with various aminoglycosides substrates reveals an enzyme with broad specificity in both enzymatic activities, accounting for AAC(6')-APH(2")'s dramatic negative impact on clinical aminoglycoside therapy. Both lividomycin A and paromomycin, aminoglycosides lacking a 6'-amino group, were acetylated by AAC(6')-APH(2"). The infrared spectrum of the product of paromomycin acetylation yielded a signal consistent with O-acetylation. Mass spectral and nuclear magnetic resonance analysis of the products of neomycin phosphorylation indicated that phosphoryl transfer occurred primarily at the 3'-OH of the 6-aminohexose ring A, and that some diphosphorylated material was also present with phosphates at the 3'-OH and the 3"'-OH of ring D, both unprecedented observations for this enzyme. Furthermore, the phosphorylation site of lividomycin A was determined to be the 5"-OH of the pentose ring C. CONCLUSIONS: The bifunctional AAC(6')-APH(2") has the capacity to inactivate virtually all clinically important aminoglycosides through N- and O-acetylation and phosphorylation of hydroxyl groups. The extremely broad substrate specificity of this enzyme will impact on future development of aminoglycosides and presents a significant challenge for antibiotic design.

Acetylation↗
PubMed1996

Surveillance of intestinal colonization and of infection by vancomycin-resistant enterococci in hospitalized cancer patients.

OBJECTIVE: To study epidemiologic features of and risk factors for intestinal colonization and infection by vancomycin-resistant enterococci (VRE) in cancer patients. METHODS: During a 41-month period, over 7600 fecal samples and all samples from sterile sites from hospitalized cancer patients were screened for VRE. Species were identified and isolates analyzed by pulsed-field gel electrophoresis (PFGE) of SmaI DNA restriction fragments. Antibiotic resistance was characterized by MIC determinations, and polymerase chain reaction for vanA, vanB, and vanC1 genes. Plasmid contents were analyzed before and after PstI and HindIII restriction, and by Southern hybridization with a vanA probe. Two case-control studies were performed to identify risk factors for colonization or infection by VRE, respectively. RESULTS: Eighty-two isolates were recovered from 81 patients. Most (72%) isolates were Enterococcus faecium VanA/vanA, with 37 different PFGE types, each of which was found in only one to four patients, except for type P1, which was found in 20 patients hospitalized over a 3-month period in the pediatric wards. Plasmid analysis suggested that only two types of plasmid were carrying gene vanA, as part of a transposon related to transposon Tn 1546 from reference strain E. faecium BM4147. Seventy-seven patients were colonized during the study period. Six of them became infected. Four patients were infected but not colonized. Only one patient died during the course of infection, but intestinal colonization persisted for months in the survivors. Case-control analysis revealed that cephalosporin treatment was a significant risk factor for colonization. No significant risk factor for infection was found in colonized patients. CONCLUSION: Colonization by VRE was mostly endemic and the colonized patients were not often infected. However, when clustered cases of colonization occurred, they were then associated with an increased rate of infection.

Journal Article↗
PubMed2000

Linkage of determinants for streptogramin A, macrolide-lincosamide-streptogramin B, and chloramphenicol resistance on a conjugative plasmid in Enterococcus faecium and dissemination of this cluster among streptogramin-resistant enterococci.

A new streptogramin A resistance gene, satG (= vatE), has been recently identified in Enterococcus faecium UW1965 (Werner and Witte 1999. Antimicrob. Agents Chemother. 43: 1813-1814). Further sequence analysis of this plasmid revealed that vatE is in a cluster together with other resistance genes. The identified ORFs were nearly identical with the already known genes ermB and cat. The ermB fragment exhibited more than 99% identity with a resistance region from the streptococcal plasmid pIP501, whereas the cat fragment also contained a truncated rep gene homologue with more than 99% identity to sequences in small staphylococcal plasmids. The cat-rep and the ermB-vatE segments were linked by an IS1216V insertion sequence widely distributed among enterococci. PCR analysis of additional 76 streptogramin-resistant isolates possessing vatE and ermB revealed a linkage of both genes in 45 isolates (59%); 15 of them with a gene arrangement, cat-repU-IS1216V-ermB-vatE, identical to the reference strain UW1965. An identical linkage of IS1216V-ermB-vatE was found among isolates from poultry manure, poultry meat, stool samples of humans, and hospital patients indicating a possible spread of the resistance gene cluster via the food chain to humans.

Anti-Bacterial Agents↗
PubMed2005

Impact of a series of interventions in vancomycin prescribing on use and prevalence of vancomycin-resistant enterococci.

BACKGROUND: In response to vancomycin-resistant bacteria, particularly vancomycin-resistant enterococci (VRE), measures have been recommended to improve on the appropriate use of vancomycin. METHODS: Intervention 1 consisted of an automatic 72-hour vancomycin stop order; Intervention 2, a standardized procedure for sampling of blood cultures; and Intervention 3, an interdisciplinary critical care team. RESULTS: After Intervention 1, inappropriate use decreased, particularly in treatment of febrile neutropenia and undocumented gram-positive infections. After Intervention 2, the baseline rate of inappropriately drawn blood cultures (IDBCs) was unchanged, and use in patients with IDBCs was comparable during both periods. Before Intervention 3, 38/55 orders continuing > 72 hours were considered inappropriate versus 24/53 (p < .025) after. After the interventions, hospitalwide vancomycin use was reduced. Yet the overall rate of VRE infection initially decreased but then increased once again over time. DISCUSSION: Despite substantial reduction in hospitalwide vancomycin use, the impact on the overall rate of VRE was inconsistent and ward dependent.

California↗
PubMed2002

The epidemiology of glycopeptide-resistant enterococci on a haematology unit--analysis by pulsed-field gel electrophoresis.

As part of an interventional study to determine glycopeptide-resistant enterococci (GRE) acquisition on a three-ward haematology unit, rectal swabs were taken weekly from 293 patients recruited to the study between June 1995 and December 1996. The GRE isolates obtained from the first positive rectal swab from 120 colonized patients, the isolates from 7 patients with clinical infection and 43 isolates obtained from the ward environment were compared by pulsed-field gel electrophoresis (PFGE). Sixty-three of 120 patients were colonized by one of strains A-H, while 49 were colonized by unique strains. The first 18 weeks were associated with the highest prevalence of GRE by rectal swab, with a single strain A responsible for 52% of acquisitions on ward 2, 22% on ward 3 and 36% on ward 4. Other smaller ward associated clusters were evident. Environmental sampling of ward 2 during this time showed that all but 2 of 30 isolates were indistinguishable from strain A. As the GRE prevalence fell, rectal swab and environmental isolates became more heterogeneous, and strain A disappeared after week 55. GRE prevalence rose again in the final 15 weeks of the study, and a new predominant strain B emerged on ward 2 responsible for 50% of new acquisitions. In the seven patients with clinical infection with GRE, the clinical isolates were compared with the contemporaneous rectal swab isolate, and were found to be the same in only two cases. An analysis of five long-term carriers colonized for a median of 19 weeks (range 11-34) showed colonization with at least two and in one case six distinct strains, raising the question of how many strains may be colonizing a patient at any one time, and suggesting that multiple colonies should be analysed. These data suggest that cross-infection was an important factor in the spread of GRE when the colonization rate was high.

Anti-Bacterial Agents↗
PubMed1999

Determinants for differential effects on D-Ala-D-lactate vs D-Ala-D-Ala formation by the VanA ligase from vancomycin-resistant enterococci.

Bacteria with either intrinsic or inducible resistance to vancomycin make peptidoglycan (PG) precursors of lowered affinity for the antibiotic by switching the PG-D-Ala-D-Ala termini that are the antibiotic-binding target to either PG-D-Ala-D-lactate or PG-D-Ala-D-Ser as a consequence of altered specificity of the D-Ala-D-X ligases in the cell wall biosynthetic pathway. The VanA ligase of vancomycin-resistant enterococci, a D-Ala-D-lactate depsipeptide ligase, has the ability to recognize and activate the weak nucleophile D-lactate selectively over D-Ala(2) to capture the D-Ala(1)-OPO(3)(2)(-) intermediate in the ligase active site. To ensure this selectivity in catalysis, VanA largely rejects the protonated (NH(3)(+)) form of D-Ala at subsite 2 (K(M2) of 210 mM at pH 7.5) but not at subsite 1. In contrast, the deprotonated (NH(2)) form of D-Ala (K(M2) of 0.66 mM, k(cat) of 550 min(-)(1)) is a 17-fold better substrate compared to D-lactate (K(M) of 0.69 mM, k(cat) of 32 min(-)(1)). The low concentration of the free amine form of D-Ala at physiological conditions (i.e., 0.1% at pH 7.0) explains the inefficiency of VanA in dipeptide synthesis. Mutational analysis revealed a residue in the putative omega-loop region, Arg242, which is partially responsible for electrostatically repelling the protonated form of D-Ala(2). The VanA enzyme represents a subfamily of D-Ala-D-X ligases in which two key active-site residues (Lys215 and Tyr216) in the active-site omega-loop of the Escherichia coli D-Ala-D-Ala ligase are absent. To look for functional complements in VanA, we have mutated 20 residues and evaluated effects on catalytic efficiency for both D-Ala-D-Ala dipeptide and D-Ala-D-lactate depsipeptide ligation. Mutation of Asp232 caused substantial defects in both dipeptide and depsipeptide ligase activity, suggesting a role in maintaining the loop position. In contrast, the H244A mutation caused an increase in K(M2) for D-lactate but not D-Ala, indicating a differential role for His244 in the recognition of the weaker nucleophile D-lactate. Replacement of the VanA omega-loop by that of VanC2, a D-Ala-D-Ser ligase, eliminated D-Ala-D-lactate activity while improving by 3-fold the catalytic efficacy of D-Ala-D-Ala and D-Ala-D-Ser activity.

Adenosine Triphosphatases↗
PubMed2003

Escherichia coli and enterococci at beaches in the Grand Traverse Bay, Lake Michigan: sources, characteristics, and environmental pathways.

This study quantified Escherichia coli (EC) and enterococci (ENT) in beach waters and dominant source materials, correlated these with ambient conditions, and determined selected EC genotypes and ENT phenotypes. Bathing-water ENT criteria were exceeded more frequently than EC criteria, providing conflicting interpretations of water quality. Dominant sources of EC and ENT were bird feces (10(8)/d/bird), storm drains (10(7)/d), and river water (10(11)/d); beach sands, shallow groundwater and detritus were additional sources. Beach-water EC genotypes and ENT phenotypes formed clusters with those from all source types, reflecting diffuse inputs. Some ENT isolates had phenotypes similar to those of human pathogens and/or exhibited high-level resistance to human-use antibiotics. EC and ENT concentrations were influenced by collection time and wind direction. There was a 48-72-h lag between rainfall and elevated EC concentrations at three southern shoreline beaches, but no such lag at western and eastern shoreline beaches, reflecting the influence of beach orientation with respect to cyclic (3-5 d) summer weather patterns. In addition to local contamination sources and processes, conceptual or predictive models of Great Lakes beach water quality should consider regional weather patterns, lake hydrodynamics, and the influence of monitoring method variables (time of day, frequency).

DNA, Bacterial↗
PubMed2005

Tidal forcing of enterococci at marine recreational beaches at fortnightly and semidiurnal frequencies.

Marine beach water quality is typically monitored in early morning once a week without respect to tidal condition. To assess the effect of tide on this public health warning system, we analyzed enterococci (ENT) data from 60 southern California marine beaches with differing geomorphology, orientation, and proximity to runoff sources. ENT concentrations during spring tides were significantly higher (p < 0.1) than those during neap tides at 50 of the beaches, and at the majority of these, water samples were also more than twice as likely to be out of compliance with the ENT single-sample standard during spring tides compared to neap tides. When tide range (spring/neap) and tide stage (ebb/flood) conditions were considered together, spring-ebb tides yielded the highest ENT concentrations and the greatest chance of exceeding the single-sample standard at the majority of beaches. The proximity to a terrestrial runoff source, the slope of the runoff source, the slope of the beach, and the orientation of the beach had minimal influence on the tidal modulation of ENT concentrations. The presence of spring and spring-ebb tide signals at such a great percentage of beaches suggests that tide should be considered in the design and interpretation of beach monitoring program data. It also suggests that ENT delivered by tidally forced sources other than terrestrial surficial runoff are widespread. Possibilities include ENT-laden groundwater (saline and fresh) from the beach aquifer as well as ENT-enriched sands, decaying wrack, and bird feces near the high water line.

Bathing Beaches↗
PubMed2006

Enterococci predictions from partial least squares regression models in conjunction with a single-sample standard improve the efficacy of beach management advisories.

Beach health advisories are issued if enterococci (ENT) densities exceed the 30-d geometric mean or single-sample water quality criteria. Current ENT enumeration procedures require 1 day of incubation; therefore, beach managers make policy decisions using 1-day-old data. This is tantamount to using a model that assumes ENT density on day t is equal to ENT density on day t-1. Research has shown that ENT densities vary over time scales shorterthan a day, calling into question the usefulness of the current model for decision-making. We created Dynamic Partial Least Square Regression (DPLSR) models for ENT at water quality monitoring stations within two adjacent marine recreational sites, Huntington State Beach (HSB) and Huntington City (HCB) Beach, California, using publicly available environmental data and tested whether these models overcome the drawbacks of the current model. The DPLSR models provide a better prediction of ENT than the current models based on comparisons of root-mean-square errors of prediction and the numbers of type 1 and 2 errors. We compared outcomes in terms of predicted illness, swimmers deterred from entering the water, and net benefits to swimmers for hypothetical management scenarios where beach advisories were issued based on (a) the previously collected sample's ENT density in conjunction with the two water quality criteria, and (b) predictions from DPLSR models in conjunction with the single-sample standard. At both HSB and HCB the DPLSR scenario produced a more favorable balance between illness prevention and recreational access. The results call into question the current method of beach management and show that model-informed decision-making and elimination of the geometric mean standard will aid beach managers in achieving more favorable outcomes in terms of illness and access than are presently achieved using 1-day-old measurements, especially at beaches where water quality problems are chronic.

Animals↗