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PubMed2000

Treatment and prevention of antibiotic associated diarrhea.

Mild or severe episodes of antibiotic-associated diarrhea (AAD) are common side effects of antibiotic therapy. The incidence of AAD differs with the antibiotic and varies from 5 to 25%. The major form of intestinal disorders is the pseudomembranous colitis associated with Clostridium difficile which occurs in 10-20% of all AAD. In most cases of AAD discontinuation or replacement of the inciting antibiotic by another drug with lower AAD risk can be effective. For more severe cases involving C. difficile, the treatment of diarrhea requires an antibiotic treatment, with glycopeptides (vancomycin) or metronidazole. Another approach to AAD treatment or prevention is based on the use of non-pathogenic living organisms, capable of re-establishing the equilibrium of the intestinal ecosystem. Several organisms have been used in treatment or prophylaxis of AAD such as selected strains of Lactobacillus acidophilus, L. bulgaricus, Bifidobacterium longum, and Enterococcus faecium. Another biotherapeutic agent, a non-pathogenic yeast, Saccharomyces boulardii has been used. In animal models of C. difficile colitis initiated by clindamycin, animals treated with S. boulardii (at end of vancomycin therapy) had a significant decrease in C. difficile colony-forming units, and of toxin B production. In several clinical randomised trials (versus placebo), S. boulardii has demonstrated its effectiveness by decreasing significantly the occurrence of C. difficile colitis and preventing the pathogenic effects of toxins A and B of C. difficile. It has been shown to be a safe and effective therapy in relapses of C. difficile colitis. A good response has been seen in children with AAD, treated by S. boulardii only. In ICUs prevention of AAD remains based on limitation of antibiotic overuse and spread of C. difficile or other agents of AAD should be prevented by improved hygiene measures (single rooms, private bathrooms for patients, use of gloves and hand washing for personnel). In addition the increasing use of biotherapeutic agents such as S. boulardii should permit the prevention of the major side effect of antibiotics, i.e. AAD in at risk patients.

Anti-Bacterial Agents↗
PubMed1999

Antiviral activity of enterocin CRL35 against herpesviruses.

Enterocin CRL35 is an antibacterial polypeptide of 3.5 x 10(3) Da produced by Enterococcus faecium CRL35. A series of experiments are described that show the enterocin also had antiviral activity against thymidine-kinase positive (tk+) and deficient (tk-) strains of herpes simplex (HSV) type 1 and 2 in Vero and BHK-21 cells. This activity was observed at 100 microg/ml, 15-fold lower than the cytotoxic concentration. In both cell lines there was a 2 log inhibition of infectivity. The compound inhibited viral multiplication in a dose-dependent manner and had no virucidal effect. Enterocin CRL35 also inhibited the virion-associated host shutoff in infected Vero cells showing that intracellular viral multiplication was affected.

Acyclovir↗
PubMed1999

Antimicrobial activity of quinupristin/dalfopristin, a new injectable streptogramin with a wide Gram-positive spectrum.

Quinupristin/dalfopristin (Synercid) is a new injectable streptogramin antibiotic proposed for the treatment of severe antimicrobial infections, that has been shown to be active against Gram-positive, multi-resistant cocci. We compared the in vitro activity of quinupristin/dalfopristin with that of amoxycillin, ampicillin, penicillin, cefixime, ceftriaxone, clindamycin, erythromycin, imipenem, meropenem, oxacillin, piperacillin/tazobactam, teicoplanin and vancomycin. The susceptibility of 37 Staphylococcus aureus (14 MS, 23 MR), 26 Staphylococcus epidermidis (16 MS, 10 MR), 20 Streptococcus pneumoniae, 33 Group A Streptococcus pyogenes, 15 Streptococcus agalactiae, 10 Enterococcus faecalis (1 vancomycin-resistant), 15 Enterococcus faecium (9 van A) was evaluated. Quinupristin/dalfopristin was active against all Gram-positive species tested, including met-R S. aureus (MIC < or = 2 mg/l), met-R S. epidermidis (MIC < or = 2 mg/l), S. pneumoniae (MIC < or = 1 mg/l), ery-R and ery-S streptococci (MIC < or = 1 mg/l). The strains of E. faecalis were generally less susceptible. Time-kill studies confirmed that quinupristin/dalfopristin at 4 x MIC concentration showed a complete bactericidal effect (3 log reduction) in about 4 6 h against all strains tested. A post-antibiotic effect (PAE) of 3.9-5.2 h was observed at 4 x MIC concentration of quinupristin/dalfopristin against staphylococci. A prolonged PAE was obtained for S. pneumoniae (8 h), S. pyogenes (9 h) and S. agalactiae (7 h), while the shortest PAE was seen for E. faecalis and E. faecium (about 4 h).

Anti-Bacterial Agents↗
PubMed2002

Functional analysis of the lipoglycodepsipeptide antibiotic ramoplanin.

The peptide antibiotic ramoplanin is highly effective against several drug-resistant gram-positive bacteria, including vancomycin-resistant Enterococcus faecium (VRE) and methicillin-resistant Staphylococcus aureus (MRSA), two important opportunistic human pathogens. Ramoplanin inhibits bacterial peptidoglycan (PG) biosynthesis by binding to Lipid intermediates I and II at a location different than the N-acyl-D-Ala-D-Ala dipeptide site targeted by vancomycin. Lipid I/II capture physically occludes these substrates from proper utilization by the late-stage PG biosynthesis enzymes MurG and the transglycosylases. Key structural features of ramoplanin responsible for antibiotic activity and PG molecular recognition have been discovered by antibiotic semisynthetic modification in conjunction with NMR analyses. These results help define a minimalist ramoplanin pharmacophore and introduce the possibility of generating ramoplanin-derived peptide or peptidomimetic antibiotics for use against VRE, MRSA, and related pathogens.

Anti-Bacterial Agents↗
PubMed1996

Synthesis and evaluation of inhibitors of bacterial D-alanine:D-alanine ligases.

BACKGROUND: D-Alanine:D-alanine ligase is essential for bacterial cell wall synthesis, assembling one of the subunits used for peptidoglycan crosslinking. The resulting aminoacyl-D-Ala-D-Ala strand is the Achilles' heel of vancomycin-susceptible bacteria; binding of vancomycin to this sequence interferes with crosslinking and blocks cell-wall synthesis. A mutant enzyme (VanA) from vancomycin-resistant Enterococcus faecium has been found to incorporate alpha-hydroxy acids at the terminal site instead of D-Ala; the resulting depsipeptides do not bind vancomycin, yet function in the crosslinking reaction. To investigate the binding specificity of these ligases, we examined their inhibition by a series of substrate analogs. RESULTS: Phosphinate and phosphonate dipeptide analogs (which, after phosphorylation by the enzyme, mimic intermediates in the ligation reaction) were prepared and evaluated as reversible inhibitors of the wild-type ligases DdlA and DdlB from Escherichia coli and of the mutant enzyme VanA. Ki values were calculated for the first stage of inhibitor binding according to a mechanism in which inhibitor competes with D-Ala for both substrate binding sites. DdlA is potently inhibited by phosphinates but not by phosphonates, while DdlB and VanA show little discrimination; both series of compounds inhibit DdlB strongly and VanA weakly. CONCLUSIONS: VanA has greatly reduced affinity for all the ligands studied. The relative affinities of the inhibitors in the reversible binding step are not, however, consistent with the substrate specificities of the enzymes. We propose a mechanism in which proton transfer from the attacking nucleophile to the departing phosphate occurs directly, without intervention of the enzyme.

Bacteria↗
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↗
PubMed2003

Probiotics, antibiotic-associated diarrhoea and Clostridium difficile diarrhoea in humans.

Probiotics are living organisms which, when ingested, have a beneficial therapeutic effect. Examples are bacteria, especially Lactobacillus rhamnosus GG, and the yeast Saccharomyces boulardii. Controlled trials indicate a benefit of both of these in the prevention of antibiotic-associated diarrhoea. Other less effective probiotics are Lactinex, Enterococcus faecium and bifidobacteria. In the difficult clinical problem of recurrent Clostridium difficile disease, S. boulardii as an adjunct to antibiotics has shown benefit in controlled trials. There is, however, less convincing evidence for the efficacy of Lactobacillus GG in this disease. Additional controlled trials and safety studies are needed before there can be a widespread endorsement of probiotics for these two conditions.

Animals↗
PubMed2002

Probiotics in antibiotic-associated diarrhoea.

Antibiotic-associated diarrhoea is a common event. In some cases, it could represent a life-threatening event. Clostridium difficile colitis is a further distinct complication of antibiotic administration. Treatment options for antibiotic-associated diarrhoea and Clostridium difficile colitis include supplementation with several types of probiotics, as overviewed in this paper. Three randomised, double-blind, controlled clinical trials show a therapeutic effect of Saccharomyces boulardii in antibiotic-associated diarrhoea. The efficacy of Lactobacillus acidophilus and bulgaricus has also been ascertained in two double-blind controlled studies. Other studies focusing on Lactobacillus as a new preventive agent for antibiotic-associated diarrhoea are not double-blind. Among these, a positive effect of Lactobacillus rhamnosus GG, Bifidobacterium longum and Enterococcus faecium SF68 has been reported. Effectiveness of probiotics in antibiotic-associated diarrhoea has, therefore, a consistent scientific rationale, however few studies have performed an assessment of bacterial recovery in stools, and this approach may be helpful in deciding a more rigorous dose standardisation.

Bifidobacterium↗
PubMed2001

Chromatographic interactions between proteins and sulfoalkylbetaine-based zwitterionic copolymers in fully aqueous low-salt buffers.

Macroporous monoliths containing N,N-dimethyl-N-methacryloyloxyethyl-N-(3-sulfopropyl)ammonium betaine (SPE) have been synthesized via in situ photopolymerization, yielding a stoichiometric balance between sulfur and nitrogen in the final polymer, which is indicative of a genuine strong/strong zwitterionic character. The chromatographic properties of these zwitterionic resins were evaluated with respect to the retention behavior of inorganic ions and proteins. The weak electrostatic nature of the interaction between the sulfobetaine monoliths and proteins provided a high selectivity between basic proteins and peptides. Elution was accomplished with low-ionic-strength fully aqueous mobile phases, whereby high recovery was obtained, even for hydrophobic proteins. Chaotropic ions such as perchlorate or thiocyanate were used as mobile phase modifiers to modulate the apparent ion exchange group density, thus introducing a route for the modulation of the ionic strength that is required to competitively elute the protein. The promising features of polymeric sulfoalkylbetaine interaction layers for separation and analysis of biological extracts was also manifested in an application involving purification of biologically active peptide-pheromone obtained from Enterococcus faecium.

Journal Article↗
PubMed2000

Peptide analogues of the VanS catalytic center inhibit VanR binding to its cognate promoter.

The dodecamer peptide SLCHDSVIGWEC, named E12, was selected from a combinatorial peptide library on the basis of its ability to bind to VanR, the two-component signal transduction response regulator which controls expression of vancomycin resistance in Enterococcus faecium. The binding of E12 was localized to the N-terminal, regulatory domain of VanR which contains Asp-55, the residue which accepts the phosphoryl group from His-164 in the activated VanS sensor kinase. E12, along with a related sequence SLAHDSIIGYLS, named E12.1, was found to inhibit the binding of VanR approximately P to a DNA segment which corresponds to its cognate promoter PvanH. With a single gap, both E12 and E12.1 could be aligned with the octadecamer sequence YLAHDIKTPLTSIIGYLS, comprising Tyr-161 through Ser-178, of the catalytic center dimerization domain of VanS, a sequence with which VanR also normally interacts. Alanine substitution analysis of E12.1 identified six amino acids as indispensable for its ability to inhibit VanR approximately P-PvanH DNA complex formation. A similar analysis of the corresponding amino acids in VanS showed a parallel dependence except for the substitutions Leu-162 --> Ala and Gly-175 --> Ala which interfered with the ability of E12.1 to compete with protein-DNA complex formation, but did not inhibit the ability of VanS to bind VanR. Our findings support a model in which E12 mimics the VanS phosphorylatable sequence with which the regulatory domain of VanR interacts, and thus functions as a "minimalist" analogue of VanS. Our results also indicate the usefulness of phage-displayed peptides as a general tool for mimicking the interacting faces of interacting proteins.

Alanine↗
PubMed1991

Identification of vancomycin resistance protein VanA as a D-alanine:D-alanine ligase of altered substrate specificity.

High-level glycopeptide resistance in Enterococcus faecium BM4147 is mediated by a 38-kDa protein VanA, whose amino acid sequence is related to Gram-negative D-alanine:D-alanine (D-Ala-D-Ala) ligases [Dutka-Malen, S., Molinas, C., Arthur, M., & Courvalin, P. (1990) Mol. Gen. Genet. 224, 364-372]. We report purification of VanA and demonstrate that it has D-Ala-D-Ala ligase activity but has substantially modified substrate specificity, compared with Gram-negative D-Ala-D-Ala ligases. VanA preferentially condenses D-Ala with D-Met or D-Phe, raising the possibility that its cellular role is to synthesize a modified cell-wall component, which is subsequently not recognized by vancomycin.

Amino Acid Sequence↗
PubMed2000

Effect of 8 week intake of probiotic milk products on risk factors for cardiovascular diseases.

OBJECTIVE: To investigate the effect of a probiotic milk product containing the culture CAUSIDO(R) and of two alternative products on risk factors for cardiovascular disease in overweight and obese subjects. DESIGN: An 8 week randomized, double-blind, placebo- and compliance-controlled, parallel study. SUBJECTS: Seventy healthy, weight-stable, overweight and obese (25.0<BMI<37.5 kg/m2) males (n=20) and females (n=50), 18-55 y old, were randomly assigned into five groups. INTERVENTION: Four groups consumed 450 ml fermented milk products (yoghurt) daily. Group 1: a yoghurt fermented with two strains of Streptococcus thermophilus and two strains of Lactobacillus acidophilus (StLa). Group 2: a placebo yoghurt fermented with delta-acid-lactone (PY). Group 3: a yoghurt fermented with two strains of Streptococcus thermophilus and one strain of Lactobacillus rhamnosus (StLr). Group 4: a yoghurt fermented with one strain of Enterococcus faecium and two strains of Streptococcus thermophilus (CAUSIDO(R) culture), GAIO(R) (G). The dietary composition of the yoghurt was otherwise similar. The fifth group was given two placebo pills (PP) daily. RESULTS: When comparing all five treatment groups, unadjusted for changes in body weight, no statistical effects were observed in week 8 in the G-group on low density lipoproteins (LDL)-cholesterol (P=0.29). After adjustment for small changes in body weight, LDL-cholesterol decreased by 8.4% (0.26+/-0.10 mmol/l; P<0.05) and fibrinogen increased (0.74+/-0.32 mmol/l; P<0.05) after 8 weeks in the G-group. This was significantly different from the group consuming chemically fermented yoghurt and the group consuming placebo pills (P<0.05). After 8 weeks, systolic blood pressure was significantly more reduced in the StLa and G-group compared to StLr. No other differences were found. CONCLUSION: The CAUSIDO(R) culture reduced LDL-cholesterol and increased fibrinogen in the overweight subjects at a 450 ml consumption daily for 8 weeks. The effect on LDL-cholesterol confirms previous studies. An immunostimulation by one of the strains in the product might explain the effect on fibrinogen in the G-group. SPONSORSHIP: MD Foods A/S, Denmark.

Adult↗
PubMed2005

Identification of glucoselysine-6-phosphate deglycase, an enzyme involved in the metabolism of the fructation product glucoselysine.

The metabolism of the glycation product fructose-epsilon-lysine in Escherichia coli involves its ATP-dependent phosphorylation by a specific kinase (FrlD), followed by the conversion of fructoselysine 6-phosphate into glucose 6-phosphate and lysine by fructoselysine-6-phosphate deglycase (FrlB), which is distantly related to the isomerase domain of glucosamine-6-phosphate synthase. As shown in the present work, several bacterial operons comprise: (1) a homologue of fructoselysine-6-phosphate deglycase; (2) a second homologue of the isomerase domain of glucosamine-6-phosphate synthase, more closely related to it; and (3) components of a novel phosphotransferase system, but no FrlD homologue. The FrlB homologue (GfrF) and the closer glucosamine-6-phosphate synthase homologue (GfrE) encoded by an Enterococcus faecium operon were expressed in E. coli and purified. Similar to FrlB, GfrF catalysed the reversible conversion of fructoselysine 6-phosphate into glucose 6-phosphate and lysine. When incubated with fructose 6-phosphate and elevated concentrations of lysine, GfrE catalysed the formation of a compound identified as 2-epsilon-lysino-2-deoxy-6-phospho-glucose (glucoselysine 6-phosphate) by NMR. GfrE also catalysed the reciprocal conversion, i.e. the formation of fructose 6-phosphate (but not glucose 6-phosphate) from glucoselysine 6-phosphate. The equilibrium constant of this reaction (0.8 M) suggests that the enzyme serves to degrade glucoselysine 6-phosphate. In conclusion, GfrF and GfrE serve to metabolize glycation products formed from lysine and glucose (fructoselysine) or fructose (glucoselysine), via their 6-phospho derivatives. The latter are presumably formed by the putative phosphotransferase system encoded by gfrA-gfrD. The designation gfr (glycation and fructation product degradation) is proposed for this operon. This is the first description of an enzyme participating in the metabolism of fructation products.

Amino Acid Sequence↗
PubMed2001

The DUEL study: a multi-center in vitro evaluation of linezolid compared with other antibiotics in the Netherlands.

OBJECTIVE: To evaluate bacterial susceptibility to linezolid in the Netherlands in comparison with other antibiotics. METHODS: Bacterial strains were isolated between September 1999 and January 2000 from patients presumed to require antibiotic treatment. The in vitro activity of 1226 strains from 34 participating laboratories was tested against linezolid, vancomycin, teicoplanin, oxacillin, penicillin, erythromycin, ampicillin and other antibiotics against enterococci, coagulase-negative staphylococci, Staphylococcus aureus and Streptococcus pneumoniae. Minimal inhibitory concentrations (MIC) were obtained with the E test on Mueller-Hinton agar: every laboratory included control strains. For vancomycin and teicoplanin only, brain-heart infusion agar and an inoculum of 2.0 McFarland was used for Staphylococcus aureus, coagulase-negative staphylococci and enterococci to support a better growth and clear recognition of hetero-resistant colonies. RESULTS: The values of MIC90 for linezolid were 1.5, 0.75, 0.75 and 1 mg/L for Staphylococcus aureus, coagulase-negative staphylococci, Streptococcus pneumoniae and enterococci, respectively. Six enterococcal strains with decreased susceptibility against vancomycin or teicoplanin were identified as Enterococcus faecium, E. gallinarum and E. casseliflavus (two strains each) and they were found to harbor vanA, vanC1 and vanC2/3 genes, respectively. Nine per cent of Streptococcus pneumoniae (an increase from 1% 4 years ago) showed decreased susceptibility to erythromycin, of both the ermB and mefE type; there was no cross-resistance with linezolid. Twelve coagulase-negative staphylococcal strains were resistant to teicoplanin. CONCLUSION: Linezolid is a promising drug in the treatment of infections caused by Gram-positive cocci. Cross-resistance with other antibiotics tested was not found.

Acetamides↗
PubMed1997

Isolation and characterization of nisin-producing Lactococcus lactis subsp. lactis from bean-sprouts.

Bacterial isolates from bean-sprouts were screened for anti-Listeria monocytogenes bacteriocins using a well diffusion method. Thirty-four of 72 isolates inhibited the growth of L. monocytogenes Scott A. One, HPB 1688, which had the biggest inhibition zone against L. monocytogenes Scott A, was selected for subsequent analysis. Both ribotyping and DNA sequencing of 16S ribosomal RNA gene demonstrated that the isolate was Lactococcus lactis subsp. lactis. Polymerase chain reaction and nucleotide sequencing revealed that the genomic DNA of the bean-sprout isolates contained a nisin Z structural gene. In MRS broth, bean-sprout isolate HPB 1688 survived at 3-4.5 degrees C for at least 20 d, grew at 4 degrees C and produced anti-listerial compounds at 5 degrees C. When co-cultured with L. monocytogenes in MRS broth, the isolate inhibited the growth of L. monocytogenes at 4 degrees C after 14 d and at 10 degrees C after 2 d. When co-inoculated with 10(2) cells g-1 of L. monocytogenes on fresh-cut ready-to-eat Caesar salad, L. lactis subsp. lactis (10(8) cells g-1) was able to reduce the number of L. monocytogenes by 1-1.4 logs after storage for 10 d at 7 zero and 10 degrees C. A bacteriocin-producing Enterococcus faecium was also able to reduce the numbers of L. monocytogenes on Caesar salad, but did not act synergistically when co-inoculated with L. lactis subsp. lactis.

Anti-Bacterial Agents↗
PubMed2001

Linezolid: pharmacokinetic characteristics and clinical studies.

Linezolid is an oxazolidinone indicated in the treatment of nosocomial and community-acquired pneumonia, complicated and uncomplicated skin and skin structure infections and vancomycin-resistant Enterococcus infections. The drug is also approved for use in complicated skin infections and nosocomial pneumonia caused by methicillin-resistant Staphylococcus aureus, concurrent bacteremia associated with vancomycin-resistant Enterococcus faecium and concurrent bacteremia associated with community-acquired pneumonia caused by penicillin-susceptible Streptococcus pneumoniae.

Acetamides↗
PubMed2002

The role of glycopeptides in the treatment of intravascular catheter-related infections.

There is increasing concern over multiresistant staphylococcci in catheter-associated infections. Local infections due to coagulase-negative staphylococci are usually resolved by removal of the intravascular catheter. However, if the device should remain for a certain period of time, e.g. to complete a course of chemotherapy, the antibiotic lock technique with a glycopeptide should be considered. In case of septic embolism to the lung caused by a multiresistant Staphylococccus aureus or Enterococcus faecium, systemic therapy with glycopeptides, streptogramins or linezolid must be employed.

Adult↗
PubMed2002

Strategies to control antibiotic resistance.

Antibiotic resistance is becoming a worldwide concern. Antibiotic resistance may be caused by sporadic mutations, which are not important unless spread clonally. Clonal resistance may disseminate a highly resistant clone to widespread geographic areas. The most effective interventions to limit the clonal spread of resistant organisms are effective infection control measures. Hospital antibiotic formulary restriction is the only control measure with proven effectiveness to control resistance related to antibiotic use. Hospital formularies should eliminate or restrict antibiotics with a high-resistance potential (eg, ceftazidime, ciprofloxacin, and imipenem), and should be replaced with equivalent antibiotics with a low-resistance potential (eg, cefe-pime, levofloxacin, and meropenem). Such low-resistance-potential antibiotics can either prevent or eliminate resistance problems associated with Klebsiella pneumoniae, Enterobacter species, or Pseudomonas aeruginosa. High-resistance-potential antibiotics, particularly ciprofloxacin and ceftazidime, also may indirectly increase the prevalence of highly resistant organisms (eg, methicillin-resistant Staphylococcus aureus [MRSA], vancomycin-resistant enterococci [VRE]). Vancomycin use should be restricted, not because it increases enterococcal resistance per se, but because it selects out naturally resistant enterococcal strains (eg, Enterococcus faecium that are vancomycin resistant). Linezolid does not increase the prevalence of VRE. Clinicians in the outpatient setting should also preferentially use oral antibiotics with a low-resistance potential (eg, clindamycin, metronidazole, doxycycline, minocycline, fluoroquinolones except ciprofloxacin, linezolid, and oral cephalosporins) in preference to their high-resistance-potential counterparts. For antibiotic resistance control interventions to be effective, they must be applied simultaneously to all antibiotics with activity against the specific resistance pathogen at the hospital formulary level. Multiple antibiotic substitutions are usually necessary to eradicate resistance problems caused by a particular pathogen. Multiple drugs of the same spectrum and low-resistance potential are necessary to eliminate resistance problems; single antibiotic substitutions are not effective.

Drug Resistance, Bacterial↗