Emergence of Vancomycin-Resistant Enterococci.
Vancomycin vancomycin (văn'kōmī`sĭn), antibiotic resembling penicillin in the way it acts. It is derived from the bacterium Streptomyces orientalis, which was isolated from soil of India and Indonesia. and ampicillin ampicillin (ăm'pĭsĭl`ĭn), a penicillin-type antibiotic that is effective against both gram-negative microorganisms and gram-positive microorganisms such as Escherichia coli. resistance in clinical Enterococcus faecium Enterococcus faecium A nosocomial pathogen resistant to most antibiotics–eg, penicillin, teicoplanin, aminoglycosides, glycopeptides; ID of E faecium in a clinical specimen requires Pt isolation with barrier precautions. strains has developed in the past decade. Failure to adhere to strict infection control to prevent the spread of these pathogens has been well established. New data implicate im·pli·cate
tr.v. im·pli·cat·ed, im·pli·cat·ing, im·pli·cates
1. To involve or connect intimately or incriminatingly: evidence that implicates others in the plot.
2. the use of specific classes of antimicrobial agents in the spread of vancomycin-resistant enterococci enterococci
bacteria in the genus Enterococcus. (VRE VRE
VRE Vancomycin-resistent enterococcus, see there ). Extended-spectrum cephalosporins Cephalosporins Definition
Cephalosporins are medicines that kill bacteria or prevent their growth.
Cephalosporins are used to treat infections in different parts of the body—the ears, nose, throat, lungs, sinuses, and and drugs with potent activity against anaerobic bacteria Anaerobic bacteria
Bacteria that do not require oxgyen, found in low concentrations in the normal vagina
Mentioned in: Aminoglycosides, Bacterial Vaginosis, Flesh-Eating Disease, Periodontal Disease may promote infection and colonization with VRE and may exert different effects on the initial establishment and persistence of high-density colonization. Control of VRE will require better understanding of the mechanisms by which different classes of drugs promote gastrointestinal colonization.
Enterococci are important nosocomial nosocomial /noso·co·mi·al/ (nos?o-ko´me-il) pertaining to or originating in a hospital.
1. Of or relating to a hospital.
2. pathogens (1,2). Their emergence in the past two decades is in many respects attributable to their resistance to many commonly used antimicrobial agents (aminoglycosides, aztreonam, cephalosporins, clindamycin, the semi-synthetic penicillins nafcillin nafcillin /naf·cil·lin/ (naf-sil´in) a semisynthetic, acid- and penicillinase-resistant penicillin that is effective against staphylococcal infections; used as the sodium salt. and oxacillin oxacillin /ox·a·cil·lin/ (ok?sah-sil´in) a semisynthetic penicillinase-resistant penicillin used as the sodium salt in infections due to penicillin-resistant, gram-positive organisms. , and trimethoprim-sulfamethoxazole) (3). Exposure to cephalosporins is a particularly important risk factor for colonization and infection with enterococci (4-6). Thus, the era in which safe and effective cephalosporins became widely available has also been an era of enterococcal ascendance as·cen·dance also as·cen·dence
Noun 1. ascendance - the state that exists when one person or group has power over another; "her apparent dominance of her husband was really her attempt to make him pay .
Ampicillin is the therapy of choice for enterococcal infections. Ampicillin MICs for Enterococcus faecalis, the most commonly isolated enterococcal species from clinical cultures, generally are 0.5 to 4.0 [micro]g/mL, whereas for the less commonly isolated E. faecium, MICs are 4 to 8 [micro]g/mL. E. faecalis and E. faecium account for [is greater than] 95% of enterococcal isolates from clinical cultures. Low-level ampicillin resistance in enterococci is attributable to the production of a lowaffinity penicillin-binding protein (PBP PBP picture by picture (TVs and monitors)
PBP Penicillin Binding Protein
PBP Paris-Brest-Paris (bicycle race)
PBP Progressive Bulbar Palsy
PBP Pay Back Period
PBP Pay By Phone ), PBP 5 (7). PBP 5s have been identified in several enterococcal species. Those of E. faecalis, E. faecium, and the closely related E. hirae demonstrate [is less than] 75% nucleic acid nucleic acid, any of a group of organic substances found in the chromosomes of living cells and viruses that play a central role in the storage and replication of hereditary information and in the expression of this information through protein synthesis. identity, but the fact that antibodies raised against one bind to all three suggests substantial structural similarity (8).
Increased ampicillin resistance in enterococci is attributable to either the production of beta-lactamase or alterations in the expression or structure of PBP 5. Beta-lactamase production has been described almost exclusively in E. faecalis and is attributable in most cases to the acquisition of the Staphylococcus aureus Staphylococcus au·re·us
A bacterium that causes furunculosis, pyemia, osteomyelitis, suppuration of wounds, and food poisoning.
Staphylococcus aureus Staphylococcus pyogenes beta-lactamase operon (9-11). Beta-lactamase production occurs at a low level in enterococci, conferring a minor increase in MIC at standard inoculum inoculum /in·oc·u·lum/ (-ok´u-lum) pl. inoc´ula material used in inoculation.
n. pl. . MIC increases more dramatically at high inoculum, however, and animal studies suggest that expression of this determinant may affect the outcome of endocarditis endocarditis (ĕn'dōkärdī`tĭs), bacterial or fungal infection of the endocardium (inner lining of the heart) that can be either acute or subacute. (12).
Ampicillin resistance resulting from changes in PBP 5 is primarily a clinical problem in E. faecium. The first detailed information about PBP 5-mediated ampicillin resistance arose from several lines of investigation. Williamson et al. noted that penicillin resistance expressed by E. faecium was related to the amount and the affinity of PBP 5 (13). The observation that enterococci could grow normally in penicillin concentrations enough to saturate sat·u·rate
v. Abbr. sat.
1. To imbue or impregnate thoroughly.
2. To soak, fill, or load to capacity.
3. To cause a substance to unite with the greatest possible amount of another substance. all the PBPs, except PBP 5, suggested that PBP 5 was capable of carrying out all the functions necessary for cell-wall synthesis. Eliopoulos et al. derived a hypersusceptible mutant of a clinical E. faecium strain and noted that it no longer produced detectable amounts of PBP 5 (14). Subsequent studies confirmed that the lack of PBP 5 expression in this mutant was due to loss of the pbp5 gene (15). Fontana et al. described in vitro in vitro /in vi·tro/ (in ve´tro) [L.] within a glass; observable in a test tube; in an artificial environment.
In an artificial environment outside a living organism. mutants of E. hirae 9790 that expressed increased levels of resistance to ampicillin (MIC 64 [micro]g/mL) (16). These mutants were found to produce increased quantities of PBP 5. In the initially analyzed strain, increased PBP 5 production was associated with a deletion within an upstream open reading frame that was characterized as a penicillin-binding protein synthesis repressor repressor: see nucleic acid. (psr) (17). A more recent study suggests that psr may serve as a global regulator of cell-wall synthesis genes in enterococci (18).
E. faecium strains expressing very high levels of ampicillin resistance (MIC [is greater than] 128 [micro]g/mL) emerged in U.S. medical centers in the late 1980s (19). Molecular analysis of these strains suggested that the increase was attributable to mutations within the pbp5 gene, which decreased the binding affinity of PBP 5 for ampicillin (20,21). One clinical study associated colonization with ampicillin-resistant E. faecium and prior therapy with extended-spectrum cephalosporins (22).
During the late 1980s, the prevalence of methicillin-resistant staphylococci was also increasing in U.S. hospitals (1), resulting in increased use of vancomycin. The discovery that antibiotic-associated diarrhea antibiotic-associated diarrhea Antibiotic-associated colits, gastroenteritis Diarrhea caused by Clostridium difficile, most often seen in a Pt taking antibiotics; many persons infected with C difficile are asymptomatic; in others, a C difficile and pseudomembranous colitis pseudomembranous colitis Antibiotic-associated colitis, necrotizing colitis GI disease An acute illness, with often severe diarrhea that follows antibiotic therapy with ampicillin, clindamycin, metronidazole, etc, which eliminate the Pt's native bacterial flora, were due to Clostridium difficile Clostridium difficile A common cause of bacterial colitis; it is the causative agent in 99% of pseudomembranous colitis, and 20-30% of antibiotic-associated diarrhea further fueled vancomycin use (23).
Vancomycin-resistant enterococci (VRE) were first reported in 1986, nearly 30 years after vancomycin was clinically introduced. The primary inciting factor was likely the use of orally administered vancomycin for treating antibiotic-associated diarrhea in hospitals. Vancomycin resistance is conferred by one of two functionally similar operons, VanA or VanB (Figure) (24). The VanA and VanB operons are highly sophisticated resistance determinants, which suggests that they evolved in other species and were acquired by enterococci. The difference in the guanine-cytosine (G-C G-C Commandant of the Coast Guard ) content of the genes of the VanB operon (roughly 50% G-C) (25) in comparison to typical enterococcal genes (35% to 40% G-C) (3) is compelling evidence for this acquisition. The conditions that would favor substantial colonization by naturally glycopeptide-resistant species (probably streptomycetes) and persistence of enterococci include high vancomycin concentrations in the gastrointestinal tract gastrointestinal tract
The part of the digestive system consisting of the stomach, small intestine, and large intestine.
Gastrointestinal tract . Substantially high levels of glycopeptides in the gastrointestinal tract are achievable by oral administration, since these agents are not absorbed, resulting in fecal vancomycin concentrations high enough to favor colonization with vancomycin-resistant streptomycetes, but not high enough to kill the notably tolerant enterococcus enterococcus /en·tero·coc·cus/ (en?ter-o-kok´us) pl. enterococ´ci an organism belonging to the genus Enterococcus.
Enterococcus /En·tero·coc·cus/ ( . Hence, it is reasonable to presume that oral administration of glycopeptides to humans was a major factor in the emergence of vancomycin resistance in enterococci. The European VRE outbreak's apparent origin in animals (who were fed oral glycopeptides as growth promoters) further supports this scenario.
[Figure ILLUSTRATION OMITTED]
Risk Factors for Multidrug-Resistant Enterococci
More than 95% of VRE recovered in the United States are E. faecium; virtually all are resistant to high levels of ampicillin. The phenotypic association of ampicillin and vancomycin resistance is in some instances due to genetic: linkage. We reported transferable ampicillin and VanB-type vancomycin resistance from E. faecium strains isolated in northeast Ohio (26). Both pbp5 and the vanB operon were located in the chromosome and linked as a result of the insertion of a VanB transposon transposon /trans·po·son/ (trans-po´zon) a small mobile genetic (DNA) element that moves around the genome or to other genomes within the same cell, usually by copying itself to a second site but sometimes by splicing itself out of its (Tn5382) immediately downstream of pbp5 (15). Both determinants were located within a larger mobile element that was able to transfer between E. faecium strains. This larger transposon is widely disseminated; it is found in clonally unrelated E. faecium isolates from New York New York, state, United States
New York, Middle Atlantic state of the United States. It is bordered by Vermont, Massachusetts, Connecticut, and the Atlantic Ocean (E), New Jersey and Pennsylvania (S), Lakes Erie and Ontario and the Canadian province of , Pennsylvania, Florida, Missouri, Ohio, and Hawaii (27).
E. faecium is less pathogenic than E. faecalis; in fact, many VRE infections resolve without active antimicrobial-drug therapy (28). However, in specific patient populations, notably in liver transplant liver transplant Hepatic transplant Transplant surgery A procedure that replaces a cancer conquered, metabolically defeated, or substance subjugated liver with one no longer required by its owner, many of whom donate same after an MVA Diseases requiring transplant patients and patients with hematologic malignancies, VRE cause serious and often fatal disease (29,30). Therefore, it is well worth understanding the factors that promote the emergence and spread of multidrug-resistant VRE.
Frequently identified risk factors for VRE colonization and infection include prolonged hospital stays, exposure to intensive care units, transplants, hematologic malignancies, and exposure to antibiotics (31). The epidemiology of VRE spread in the hospital involves both person-to-person transmission and selective antibiotic pressure. Very specific practices designed to prevent the person-to-person spread of VRE have been recommended by the Hospital Infection Control Practices Advisory Committee to the Centers for Disease Control and Prevention Centers for Disease Control and Prevention (CDC), agency of the U.S. Public Health Service since 1973, with headquarters in Atlanta; it was established in 1946 as the Communicable Disease Center. and are in place in many hospitals (32). These measures include surveillance for colonization, identification of colonized Colonized
This occurs when a microorganism is found on or in a person without causing a disease.
Mentioned in: Isolation and infected patients, isolation or cohorting of colonized persons, strict use of gloves and gowns by people coming into contact with the patient, thorough room cleaning after patient discharge, and efforts to limit use of vancomycin in hospitals. In geographically limited outbreaks caused by the dissemination of a single VRE clone, these practices have successfully eliminated the organisms from the hospital (33-35). In larger, more disseminated outbreaks caused by several different VRE clones, infection control measures and control of vancomycin use have shown only limited efficacy, suggesting selection pressure by antimicrobial drugs other than vancomycin (36,37).
Antibiotics other than glycopeptides have been linked with increased risk for colonization and infection with VRE, most prominently, the extended-spectrum cephalosporins and antibiotics with potent activity against anaerobic bacteria (26,31,38,39). These associations have been noted in retrospective, uncontrolled studies.
Nonglycopeptide Antibiotics and VRE
Are there compelling reasons to believe that cephalosporins or antibiotics with potent activity against anaerobic bacteria increase risk for VRE? Early studies reported VRE strains in which exposure to vancomycin increased the susceptibility to beta-lactams (40). It was hypothesized that PBP 5 was unable to process peptidoglycan peptidoglycan /pep·ti·do·gly·can/ (pep?ti-do-gli´kan) a glycan (polysaccharide) attached to short cross-linked peptides; found in bacterial cell walls.
n. precursors terminating in D-lactate. Therefore, expression of vancomycin resistance, whose mechanism in both VanA and VanB strains involves the substitution of D-lactate for D-alanine at the terminus of the pentapeptide pen·ta·pep·tide
A polypeptide composed of five amino acids. precursors, would need to involve other PBPs in cell-wall synthesis. These other PBPs would be susceptible to beta-lactams, including cephalosporins. However, mutants resistant to synergism synergism /syn·er·gism/ (sin´er-jizm) synergy.
synergism are relatively easy to select in vitro, and strains resistant to such synergism are commonly found in the clinical setting (41).
The cephalosporin cephalosporin (sĕf'əlōspôr`ĭn), any of a group of more than 20 antibiotics derived from species of fungi of the genus Cephalosporium and closely related chemically to penicillin. Cephalosporins, e.g. association may be related to the fact that virtually all VRE in the United States express high-level ampicillin resistance. The high-level ampicillin-resistant strains express even higher degrees of resistance to extended-spectrum cephalosporins ([is greater than] 10,000 [micro]g/mL) (26). The concentrations of cephalosporins achievable in bile (as high as 5,000 [micro]g/mL for ceftriaxone ceftriaxone /cef·tri·ax·one/ (cef?tri-ak´son) a semisynthetic, ß–resistant, third-generation cephalosporin effective against a wide range of gram-positive and gram-negative bacteria, used as the sodium salt. ) (42-44) can inhibit or kill virtually all upper gastrointestinal bacterial flora, except for VRE. On the other hand, antienterococcal penicillins such as piperacillin, which appear to be protective against VRE in some clinical studies, achieve biliary concentrations in excess of 1,000 [micro]g/mL in human bile after standard doses (45). These concentrations exceed the MIC of most VRE for piperacillin (256 to 1024 [micro]g/mL). It is therefore within reason that the potentially protective effect observed with piperacillin is explainable by its direct inhibition of VRE in the upper gastrointestinal tract.
We tested this hypothesis in an animal model in which subcutaneous doses of different antimicrobial agents were administered to mice for 2 days, followed by intragastric injection of small numbers (ca. 100 CFU CFU
see colony-forming units. ) of a highly ampicillin-resistant VRE strain B E. faecium C68 (46). Stool samples were subsequently collected over a 2- to 3-week period to determine whether high-level VRE colonization was established. In this model, subcutaneous administration of piperacillin-tazobactam was found to protect against high-level VRE colonization, whereas ceftriaxone and ticarcillin-clavulanic acid (with antienterococcal activity equivalent to the cephalosporins) promoted high-level VRE colonization (Table 1). These results are consistent with a model in which piperacillin is protective because of direct inhibition of VRE in the upper gastrointestinal tract, whereas ceftriaxone and ticarcillin promote colonization because they inhibit everything but VRE, thereby permitting high-level colonization.
Table 1. Pretreatment with antibiotics and vancomycin-resistant enterococci (VRE) colonization after gastric administration of [10.sup.2] CFU vancomycin and ampicillin-resistant Enterococcus faecium C68 (46) Approximate [log.sub.10] CFU VRE/g stool Day 3 Day 6 Day 9 Day 13 Day 16 Saline 2 2.5 3.0 2.5 2.5 Piperacillin- 2 2 2 2 2 tazobactam Ticarcillin- >9 >9 8.2 6.8 6.8 clavulanic acid Ceftriaxone >9 8.8 8.4 7.2 6
A direct activity of antianaerobic antibiotics against VRE is more difficult to understand, since some of these antibiotics are among the most active antienterococcal agents (ampicillin-sulbactam, piperacillin-tazobactam), and most of the extended-spectrum cephalosporins have relatively weak activity against anaerobes. Conceivably, however, these antibiotics exhibit potent activity against species that successfully compete with enterococci for colonization of the gastrointestinal tract, thereby promoting persistence of high-level VRE colonization once it is successfully established. We tested this hypothesis in a separate animal model in which high-level VRE colonization was established by intragastric injection of [10.sup.6] CFU of C68 after administration of oral vancomycin (47). This technique established colonization of mouse stool with [10.sup.9] CFU of VRE in all animals. When oral vancomycin was discontinued, colonization levels declined at a regular and predictable rate; most animals had no detectable colonization after 3 weeks. We tested the effects of subcutaneous administration of different antibiotics on the persistence of high-level VRE colonization (Table 2). Vancomycin and antibiotics with potent activity against anaerobic bacteria (ampicillin-sulbactam, cefoxitin, clindamycin, metronidazole metronidazole /met·ro·ni·da·zole/ (-ni´dah-zol) an antiprotozoal and antibacterial effective against obligate anaerobes; used as the base or the hydrochloride salt. It is also used as a topical treatment for rosacea. , piperacillin-tazobactam, and ticarcillin-clavulanic acid) promoted persistence of high-level VRE colonization, even though some had excellent activity against enterococci and had been shown to prevent VRE colonization in the other model (see above). In contrast, antibiotics with relatively poor antianaerobic activity (aztreonam, cefepime, ceftriaxone, ciprofloxacin ciprofloxacin /cip·ro·flox·a·cin/ (sip?ro-flok´sah-sin) a synthetic antibacterial effective against many gram-positive and gram-negative bacteria; used as the hydrochloride salt.
n. ) did not promote high-level colonization.
Table 2. Antibiotic treatment and persistence of high-level colonization with vancomycin and ampicillin-resistant Enterococcus faecium C68 (.47) Approximate [log.sub.10] CFU VRE/g stool(a) Day 0 Day 4-5 Day 9-10 Day 14-15 Day 19-20 Saline 9.5 8.3 6 3.8 3.5 Vancomycin (SQ) >9 >9 >9 >9 >9 Vancomycin (oral) >9 >9 >9 >9 >9 Antibiotics with potent antianaerobic activity Piperacillin- >9 >9 >9 >9 >9 tazobactam Ticarcillin- >9 >9 >9 >9 >9 clavulanic acid Clindamycin >9 >9 >9 >9 >9 Cefotetan >9 >9 8.8 7.8 8 Metronidazole >9 >9 >9 >9 >9 Ampicillin >9 >9 8 7.2 7 Ampicillin- >9 >9 >9 7.8 7.7 sulbactam Antibiotics with relatively poor activity against anaerobic bacteria Cefepime >9 >9 6.2 5 4.8 Ceftriaxone >9 8.8 8.4 7.2 6 Aztreonam >9 9 4.3 4.2 3.8 Ciprofloxacin >9 8.8 6 5.2 5 (a) VRE = vancomycin-resistant enterococci; SQ = subcutaneous.
Antibiotics and VRE Colonization and Infection
The above results suggest a model for antibiotic influence on the spread of VRE. Commonly used antibiotics that achieve high gastrointestinal concentrations but are inactive against enterococci, such as the cephalosporins, ticarcillin, and perhaps vancomycin, favor colonization with high levels of VRE in the stool. Antibiotics active against anaerobic bacteria, which are the primary competitors of enterococci for colonizing the gastrointestinal tract, favor the persistence of high levels of VRE in stool but may or may not (depending on their intrinsic antienterococcal activity) favor colonization in uncolonized patients. Antibiotics that meet both criteria, such as ticarcillin-clavulanic acid, should be particularly associated with VRE. In a citywide analysis of hospitals in the greater Cleveland area, the use of ticarcillin-clavulanic acid was associated with higher hospital rates of clinical VRE (26). A positive, although not statistically significant, association was noted for extended-spectrum cephalosporins, while a negative but statistically insignificant association was noted for the combination of ampicillin, ampicillin-sulbactam, piperacillin, and piperacillin-tazobactam.
The frequent association of cephalosporins with VRE colonization and the failure to associate piperacillin-tazobactam with VRE suggest that the most important driving force for the emergence and spread of these organisms within institutions may be the predilection for establishing new colonizations. This is not to say that antimicrobial agents that promote persistence of high-level colonization will not be important for promoting VRE outbreaks, but that this effect is less pronounced if high-volume use of cephalosporins (or ticarcillin-clavulanic acid) does not create receptive new environments for establishing new colonization.
These data also suggest that refined strategies can be developed to limit the emergence and spread of VRE within hospitals. Commitment to serious infection control practices and limitation of vancomycin use must remain the cornerstones of any successful strategy. However, it is possible to envision settings where surveillance-culturing systems are taken seriously and patients who are colonized with VRE are routinely identified. In such settings, the choice of which empiric antibiotic to administer for a presumed nosocomial infection Nosocomial infection
An infection that can be acquired in a hospital. ABPA is a nosocomial infection.
Mentioned in: Allergic Bronchopulmonary Aspergillosis, Hospital-Acquired Infections, Pseudomonas Infections
would be affected by the colonization status of the patient. In patients known to be colonized with VRE, broad-spectrum agents that lack significant activity against anaerobes (such as extended-spectrum cephalosporins of fluoroquinolones) would be preferred, on the assumption that potent anaerobic anaerobic /an·aer·o·bic/ (an?ah-ro´bik)
1. lacking molecular oxygen.
2. growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. activity would not be required for treating the infection. If the patient is not colonized with VRE, administration of a potent antienterococcal broad-spectrum agent such as piperacillin-tazobactam may be preferred. In this manner, both the establishment of new colonization and the level of colonization of those already colonized could be minimized.
Multidrug-resistant enterococci continue to pose problems in U.S. medical centers. The best available evidence suggests that the emergence and spread of these pathogens are promoted by poor infection control techniques and by antibiotic selective pressure. Antibiotic selective pressure favoring the emergence and spread of VRE may involve more than simply the extent of vancomycin use. Specifically, extended-spectrum cephalosporins and similarly active beta-lactams and drugs with potent activity against anaerobes appear to predispose pre·dis·pose
To make susceptible, as to a disease. to VRE colonization and infection. On one hand, data from animal models suggest that the cephalosporins predispose to establishment of VRE colonization through their potent activity against many bacteria and essential lack of activity against ampicillin-resistant enterococci. On the other hand, antianaerobic antibiotics appear to favor persistence of high levels of VRE colonization through their activity against competing flora. A more detailed understanding of the impact of different antibiotics on the upper and lower gastrointestinal flora will be an important step in controlling the emergence and spread of VRE.
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tr.v. razed also rased, raz·ing also ras·ing, raz·es also ras·es
1. To level to the ground; demolish. See Synonyms at ruin.
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(24.) Arthur M, Reynolds P, Courvalin P. Glycopeptide resistance in enterococci. Trends Microbiol 1996;4:401-7.
(25.) Evers S, Sahm DF, Courvalin P. The vanB gene of vancomycin-resistant Enterococcus faecalis V583 is structurally related to genes encoding D-ala: D-ala ligases and glycopeptide-resistance proteins VanA and VanC. Gene 1993;124:143-4.
(26.) Donskey CJ, Schreiber JR, Jacobs MR, Shekar R, Smith F, Gordon S, et al. A polyclonal polyclonal /poly·clo·nal/ (-klon´'l)
1. derived from different cells.
2. pertaining to several clones.
derived from different cells; pertaining to several clones. outbreak of predominantly VanB vancomycin-resistant enterococci in Northeast Ohio. Clin Infect Dis 1999;29:573-9.
(27.) Hanrahan J, Hoyen C, Rice LB. Geographic distribution of a large mobile element that transfers ampicillin and vancomycin resistance between Enterococcus faecium strains. Antimicrob Agents Chemother 2000;44:1349-51.
(28.) Quale qua·le
n. pl. qua·li·a
A property, such as whiteness, considered independently from things having the property.
[From Latin qu J, Landman D, Atwood E, Kreiswirth B, Willey BM, Ditore V, et al. Experience with a hospital-wide outbreak of vancomycin-resistant enterococci. Am J Infect Control 1996;24:372-9.
(29.) Linden PK, Pasculle AW, Manez R, Kramer DJ, Fung JJ, Pinna pinna /pin·na/ (pin´ah) auricle (1).pin´nal
n. pl. pin·nae
pin AD, et al. Differences in outcomes for patients with bacteremia due to vancomycin-resistant Enterococcus faecium or vancomycin-susceptible E. faecium. Clin Infect Dis 1996;22:663-70.
(30.) Roghmann M-C, Qaiyumi S, Johnson IA, Schwalbe R, Morris JG Jr. Recurrent vancomycin-resistant Enterococcus faecium bacteremia in a leukemia patient who was persistently colonized with vancomycin-resistant enterococci for two years. Clin Infect Dis 1997;24:514-15.
(31.) Edmond MB, Ober IF, Weinbaum DL, Pfaller MA, Hwang T, Sanford MD, et al. Vancomycin-resistant Enterococcus faecium bacteremia: risk factors for infection. Clin Infect Dis 1995;20:1126-33.
(32.) Centers for Disease Control and Prevention. Preventing the spread of vancomycin resistance - report from the Hospital Infection Control Practices Advisory Committee. Federal Register 1994;59:25758-63.
(33.) Boyce JM, Opal SM, Chow JW, Zervos MI, Potter-Bynoe G, Sherman CB, et al. Outbreak of multidrug-resistant Enterococcus faecium with transferable vanB class vancomycin resistance. J Clin Microbiol 1994;32:1148-53.
(34.) Boyce JM, Mermel LA, Zervos MI, Rice LB, Potter-Bynoe G, Giogio C, et al. Controlling vancomycin-resistant enterococci. Infect Control Hosp Epidemiol 1995;16:634-7.
(35.) Boyce JM. Vancomycin-resistant enterococcus: detection, epidemiology and control measures. Infect Dis Clin North Am 1997;11:367-83.
(36.) Morris JG, Shay shay
[Back-formation from chaise (taken as pl. )]
Noun 1. DK, Hebden IN, McCarter RJ Jr, Perdue Perdue may refer to:
(37.) Slaughter S, Hayden MK, Nathan C, Hu T-C, Rice T, Van Voorhis J, et al. A comparison of the effect of universal use of gloves and gowns with that of glove use alone on acquisition of vancomycin-resistant enterococci in a medical intensive care unit. Ann Intern Med 1996;125:448-56.
(38.) Moreno F, Grota P, Crisp C, Magnon K, Melcher GP, Jorgensen IH, et al. Clinical and molecular epidemiology molecular epidemiology Molecular medicine An evolving field that combines the tools of standard epidemiology–case studies, questionnaires and monitoring of exposure to external factors with the tools of molecular biology–eg, restriction endonucleases, of vancomycin-resistant Enterococcus faecium during its emergence in a city in southern Texas. Clin Infect Dis 1995;21:1234-7.
(39.) Quale J, Landman D, Saurina G, Atwood E, DiTore V, Patel K. Manipulation of a hospital antimicrobial formulary formulary /for·mu·lary/ (for´mu-lar?e) a collection of recipes, formulas, and prescriptions.
National Formulary see under N.
n. to control an outbreak of vancomycin-resistant enterococci. Clin Infect Dis 1996;23:1020-5.
(40.) Shlaes DM, Etter L, Gutmann L. Synergistic killing of vancomycin-resistant enterococci of classes A, B and C by combinations of vancomycin, penicillin and gentamicin gentamicin /gen·ta·mi·cin/ (jen?tah-mi´sin) an aminoglycoside antibiotic complex isolated from bacteria of the genus Micromonospora, . Antimicrob Agents Chemother 1991;35:776-9.
(41.) Fraimow HS, Venuti E. Inconsistent bactericidal bactericidal /bac·te·ri·ci·dal/ (bak-ter?i-si´d'l) destructive to bacteria.
An agent that destroys bacteria (e.g. activity of triple-combination therapy with vancomycin, ampicillin and gentamicin against vancomycin-resistant, highly ampicillin resistant Enterococcus faecium. Antimicrob Agents Chemother 1992;36:1563-6.
(42.) Hayton WL, Schandlik R, Stoeckel K. Biliary excretion and pharmacokinetics of ceftriaxone after cholecystectomy Cholecystectomy Definition
A cholecystectomy is the surgical removal of the gallbladder. The two basic types of this procedure are open cholecystectomy and the laparoscopic approach. . Eur J Clin Pharmacol 1986;30:445-51.
(43.) Brogard JM, Jehl F, Paris-Bockel D, Blickle IF, Adloff M, Monteil H. Biliary elimination of ceftazidime. J Antimicrob Chemother 1987;19:671-8.
(44.) Kees F, Strehl E, Dominiak P, Grobecker H, Seeger K, Seidel sei·del
A beer mug.
[German, from Middle High German sdel, from Latin situla, bucket.]
Noun 1. G, et al. Cefotaxime and desacetyl cefotaxime in human bile. Infection 1983;11:118-20.
(45.) Taylor EW, Poxon V, Alexander-Williams J, Jackson D. Biliary excretion of piperacillin. J Int Med Res 1983; 11:28-31.
(46.) Donskey CJ, Hanrahan IA, Hutton RA, Rice LB. Effect of parenteral parenteral /pa·ren·ter·al/ (pah-ren´ter-al) not through the alimentary canal, but rather by injection through some other route, as subcutaneous, intramuscular, etc.
1. antibiotic administration on establishment of colonization with vancomycin-resistant Enterococcus faecium in the mouse gastrointestinal tract. J Infect Dis 2000;181:1830-3.
(47.) Donskey CJ, Hanrahan IA, Hutton RA, Rice LB. Effect of parenteral antibiotic administration on persistence of vancomycin-resistant Enterococcus faecium in the mouse gastrointestinal tract. J Infect Dis 1999;180:384-90.
Dr. Rice is chief of the medical service at the Louis Stokes Cleveland Veterans Administration Medical Center, vice chairman of the department of medicine at University Hospitals of Cleveland University Hospitals is a major not-for-profit medical center in Cleveland, Ohio, United States. With 150 locations throughout northeast Ohio, it encompasses a network of hospitals, outpatient centers and primary care physicians. , and professor of medicine at Case Western Reserve University. His primary research interests are in the mechanisms of antimicrobial resistance and resistance transfer in enterococci and the evolution of extended-spectrum beta-lactamases in gram-negative bacilli bacilli /ba·cil·li/ (bah-sil´i) plural of bacillus.
see bacillus. .
Address for correspondence: Louis B. Rice, Medical Service 111(W),VA Medical Center, 10701 East Blvd., Cleveland, OH 44106, USA; fax: 216-231-3289; e-mail: firstname.lastname@example.org