Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “enterococci”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 685 records · Page 38Linked to original sources

Antimicrobial susceptibility of vancomycin-susceptible and -resistant enterococci isolated in Italy from raw meat products, farm animals, and human infections.

The susceptibility of vancomycin-resistant (VRE) and vancomycin-susceptible (VSE) enterococci to 10 antimicrobial agents was evaluated. The strains, belonging to different species, were isolated in Italy from raw meat products, farm animals, and human clinical infections in the years 1997-2000. High frequency of resistance to tetracycline and erythromycin was observed in all the groups of strains. On the contrary, chloramphenicol was the only drug that showed a relatively low rate of resistance in all the groups examined. In general, the resistance rates observed for VSE did not differ from those observed for VRE of the same species and origin. Some differences could be noticed among the different enterococcal species, with Enterococcus faecium strains being usually more resistant to beta-lactams, and Enterococcus faecalis strains more resistant to gentamicin. However, the strongest differences were observed when the strains were compared according to their source, the human isolates being usually more resistant than the isolates of animal origin. No significant difference was observed between isolates of swine and poultry origin. Among VRE E. faecium, multiple resistance was much more frequent among the human strains (90%) than among poultry (48.9%) and swine (26.5%) strains. These results show that in Italy VRE isolates from human clinical infections are usually more resistant than isolates from meat products and farm animals, and possess different antimicrobial resistance profiles.

Animals↗

Antimicrobial resistance profiles of dairy and clinical isolates and type strains of enterococci.

The susceptibility to 30 antimicrobial agents was determined by the disk diffusion method for a collection of 172 enterococcal strains, including 96 isolates from dairy sources, 50 isolates of human and veterinary origin, and 26 reference strains from 24 different enterococcal species. Results were analysed by hierarchic numerical methods to cluster strains and to group antimicrobials according to similarity profiles. Resistance to 17 of the 30 antimicrobials showed to be correlated, leading to four groups reflecting the mode of action: quinolones (ofloxacin, enrofloxacin, ciprofloxacin and norfloxacin); macrolides (erythromycin, spiramycin), phenicols (cloramphenicol) and tetracyclins (tetracycline, oxytetracyclin); aminoglycosides (gentamicin, kanamycin) and lincosamides (clindamycin); penicillins (amoxicillin, ampicillin, penicillin G, piperacillin) and carbapenems (imipenem). Overall, the genus Enterococcus behaved as resistant to lincomycin, colistin, polimixin B and, with a few exceptions in dairy isolates, to methicillin. In general, all isolates were susceptible to vancomycin, cloramphenicol and fusidic acid. Clusters containing only dairy isolates were susceptible to the majority of antimicrobials tested, as opposed to clusters constituted only by clinical enterococcal isolates. Among the clinical isolates, 62% were highly multiresistant. Low level gentamicin resistance was found to be associated with clinical enterococci. Among dairy isolates, those that clustered with clinical isolates were both resistant to gentamicin and identified as Enterococcus faecalis. Resistance to macrolides, quinolones, penicillins and imipenem was found to be associated also with clinical environments, mainly with multiresistant isolates, contrary to what is generally agreed as a characteristic of the genus. Veterinary clinical isolates were mainly grouped with the multiresistant clinical human isolates. The 26 reference enterococcal strains were distributed in clusters with different antibiotic resistance profiles and were mainly clustered with dairy isolates.

Anti-Bacterial Agents↗

Antimicrobial susceptibility of enterococci strains isolated from slaughter animals on the data of Hungarian resistance monitoring system from 2001 to 2004.

Isolates of Enterococcus spp. were collected from January 2001 to December 2004 from caecal samples of slaughtered poultry, swine and cattle in Hungary. The isolates were identified by their growth and biochemical properties and with PCR. The antibiotic susceptibility of a total number of 1272 isolates was tested with disk diffusion test to ampicillin, gentamicin, streptomycin, tetracycline, erythromycin and vancomycin. It was established that although ampicillin and amoxicillin are often used in veterinary practice its resistance rate was relatively low. In the case of tetracyclines and macrolides, a high incidence of resistance was found. Susceptibility of strains to tetracyclines and/or macrolides reduced in both 2003 and 2004 in all animal species, which may be due to the more frequent usage of these drugs in the veterinary practice following the ban of growth promoters. The annual data of vancomycin resistance point to an association between the recovery of vancomycin-resistant enterococci (VRE) isolates and the use of avoparcin. This study indicates that reducing antimicrobial resistance in food animals could be possible with lower usage of antibiotics, although variations can occur with different strains.

Abattoirs↗

Implications of colonization of vancomycin-resistant enterococci (VRE) in renal dialysis patients. Learning to live with it?

Vancomycin-resistant enterococci (VRE) commonly colonize, but less frequently infect, debilitated patients, such as those on chronic renal dialysis. The emergence of VRE amongst our cohort of renal replacement therapy patients posed considerable challenges in our attempts to prevent spread. Although 60 of 451 (13%) patients became colonized, only two patients required systemic antibiotics for confirmed or suspected invasive infection. Mortality and inpatient stay was greater in VRE-positive compared with VRE-negative patients (50% versus 10%) and patients who were screened on three or more occasions were likely to remain positive (e.g. 56% of patients screened on six occasions were positive). The application of recommended guidelines for the control of VRE, however, severely disrupted our renal dialysis programme and therefore had to be abandoned. As patients on renal dialysis are more likely to acquire VRE, remain colonized, require antibiotics and require regular inpatient or outpatient care more frequently than other patients, control measures should be adapted to minimize spread but not disrupt important and essential medical services.

Adolescent↗

Control of vancomycin-resistant enterococci in a hospital: a five-year experience in a Taiwanese teaching hospital.

In order to prevent transmission of hospital-acquired vancomycin-resistant enterococci (VRE), the infection control team (ICT) of the National Taiwan University Hospital (NTUH) introduced practical guidelines from January 1997 to June 2000. All patients at NTUH found to be infected or colonized with VRE were placed in strict contact and cohort isolation. Surveillance cultures were obtained from other patients in close proximity in order to determine any spread of VRE. If identified, these patients were also placed in contact and cohort isolation, and their isolates were subjected to antimicrobial susceptibility testing and molecular typing by pulsed-field gel electrophoresis. During this period, 20 patients were found to have VRE. Based on typing results, there were three occasions where the same VRE strain had spread between index patients and roommates or patients staying in neighbouring rooms. No further spread occurred after applying strict contact isolation for these patients. The hospital-acquired VRE infection rate was around 0.03 to 0.09 per 1000 discharges during the intervention period. After July 2000, however, members of the ICT did not actively monitor or implement any interventions to control VRE. The rate then increased to 0.20 per 1000 discharges in 2001. This study suggests that interventions for the control of VRE, based on the guidelines from the Hospital Infection Control Practice Advisory Committee, are effective for control of VRE spread. Failure to adhere to these guidelines may result in an increase in hospital-acquired VRE.

Adolescent↗

Colonization by high-level aminoglycoside-resistant enterococci in intensive care unit patients: epidemiology and clinical relevance.

A cohort study was performed to investigate the risk factors for colonization with high-level aminoglycoside-resistant enterococci (HLARE) in intensive care unit (ICU) patients. Colonization was investigated by performing surveillance samples during ICU stay. Clonal relatedness of the isolates was assessed by pulsed-field gel electrophoresis. Eighty-six patients with an ICU stay of >48 h were included; two were colonized with HLARE at admission, and 24 (28.5%) acquired HLARE during their stay in the ICU. HLARE were initially isolated from rectal swabs alone. Thirty-five percent of Enterococcus faecalis and 57% of E. faecium showed high-level resistance to gentamicin or streptomycin. Most isolates were clonally unrelated. Using multi-variate analysis, the only variable associated with HLARE colonization was previous antimicrobial use. Five patients had HLARE isolated from clinical samples, three of them with infection; in all of these, colonization with the same clone had been detected previously by surveillance samples. We conclude that most infections due to HLARE in the ICU are preceded by previous colonization, and that antimicrobial use is the main risk factor for colonization.

Aminoglycosides↗

Guidelines for the control of glycopeptide-resistant enterococci in hospitals.

The increase since the mid 1980s in glycopeptide resistant enterococci (GRE) raised concerns about the limited options for antimicrobial therapy, the implications for ever-increasing numbers of immunocompromised hospitalised patients, and fuelled fears, now realised, for the transfer of glycopeptide resistance to more pathogenic bacteria, such as Staphylococcus aureus. These issues underlined the need for guidelines for the emergence and control of GRE in the hospital setting. This Hospital Infection Society (HIS) and Infection Control Nurses Association (ICNA) working party report reviews the literature relating to GRE prevention and control. It provides guidance on microbiological investigation, treatment and management, including antimicrobial prescribing and infection control measures. Evidence identified to support recommendations has been categorized. A risk assessment approach is recommended and areas for research and development identified.

Anti-Bacterial Agents↗

Antibacterial activity of alpha-mangostin against vancomycin resistant Enterococci (VRE) and synergism with antibiotics.

alpha-Mangostin, isolated from the stem bark of Garcinia mangostana L., was found to be active against vancomycin resistant Enterococci (VRE) and methicillin resistant Staphylococcus aureus (MRSA), with MIC values of 6.25 and 6.25 to 12.5 microg/ml, respectively. Our studies showed synergism between alpha-mangostin and gentamicin (GM) against VRE, and alpha-mangostin and vancomycin hydrochloride (VCM) against MRSA. Further studies showed partial synergism between alpha-mangostin and commercially available antibiotics such as ampicillin and minocycline. These findings suggested that alpha-mangostin alone or in combination with GM against VRE and in combination with VCM against MRSA might be useful in controlling VRE and MRSA infections.

Anti-Bacterial Agents↗

Antimicrobial activity of isoprenoid-substituted xanthones from Cudrania cochinchinensis against vancomycin-resistant enterococci.

Ten xanthones with one or two isoprenoid groups and a prenylated benzophenone isolated from roots of Cudrania cochinchinensis (Moraceae) were tested for their antimicrobial activities against vancomycin-resistant enterococci (VRE). Among these compounds, gerontoxanthone H exhibited considerable antibacterial activity against five VRE strains (VanA, VanB and VanC) (MICs = 1.56 microg/ml). Four xanthones, 1,3,7-trihydroxy-2-prenylxanthone, gerontoxanthone I, alvaxanthone and isoalvaxanthone, showed weaker antibacterial activity against these VREs (MICs = 3.13-6.25 microg/ml). .

Anti-Bacterial Agents↗

Clinical glycopeptide-resistant enterococci isolated from patients after solid organ transplantation.

The aim of this study was to confirm the identification and resistance to vancomycin and teicoplanin of nosocomial enterococcal strains using molecular biology methods. Glycopeptide-resistant enterococci (GRE) strains were isolated from clinical specimens of hospitalized patients. Bacterial identification was performed in an automatic ATB Expression system (bioMérieux SA). Susceptibility to glycopeptides was determined by the disc diffusion method and Etest (AB BIODISK, Sweden). We performed polymerase chain reactions (PCR) for Enterococcus faecium and E. faecalis identification and van genes detection. Fifteen GRE strains were cultured over 2 years (2003-2004). Fourteen isolates were highly resistant to vancomycin (MIC range, 128->256 mg/L) and teicoplanin (MIC range, 32->256 mg/L). Twelve strains harbored van A gene (Van A phenotype). Seven isolates were identified as E. faecium and seven as E. faecalis by the multiplex-PCR method. One strain-E. casseliflavus-showed low resistance to vancomycin (MIC 8 mg/L) with retained susceptibility to teicoplanin (MIC 4 mg/L). It harbored the van C2/C3 gene and was identified as the Van C2/C3 phenotype. GRE strains were more often isolated from hospitalized patients in Poland. Constant monitoring by reliable microbiological methods has become necessary to prevent the spread of these strains in the hospital environment.

Drug Resistance↗

An analytical model of enterococci inactivation, grazing, and transport in the surf zone of a marine beach.

An analytical model of enterococci (ENT) concentrations in the surf zone of a long sandy beach is constructed considering the physical processes of dilution by rip currents and alongshore littoral drift, and the biological processes of inactivation and mortality by grazing. The solution is used to construct an expression for the length of shoreline adversely impacted by ENT from a point source. Two non-dimensional parameters are developed whose magnitude can be used to ascertain whether dilution, inactivation, or grazing is the dominant sink for ENT in the surf zone. The model is applied to beaches in southern California, USA. Model input parameters related to physical processes and inactivation are compiled from the literature. Laboratory experiments are conducted to determine grazing mortality rates of ENT (6.5 x 10(-6) s(-1)). Results indicate that at the field sites, between 1000 and 5000 m of shoreline are typically impacted by a continuous point source of ENT. Dilution is the primary cause of decline in ENT concentrations within the surf zone, with inactivation secondary and grazing tertiary. Results recommend strategic positioning of point sources and timing of effluent releases to take advantage of high dilution conditions. Our estimates for grazing mortality rates are within the same order of magnitude as some published inactivation rates, thus we cannot rule out the possibility that grazing is an important sink for ENT, especially in low dilution environments like enclosed bays.

Bathing Beaches↗

Vancomycin-resistant enterococci: clinical, microbiologic, and epidemiologic features.

Enterococci have emerged as important nosocomial pathogens with increasing antimicrobial resistance. Within the past 5 years, vancomycin-resistant strains have disseminated throughout the United States and Europe. Many of these organisms are also highly resistant to beta-lactams and aminoglycosides, making them virtually untreatable. Because optimal therapy for these infections is unknown, attributable mortality rates for patients with vancomycin-resistant enterococcal bacteremia are extremely high. Recently identified risk factors for acquisition include prolonged hospitalization, prior antibiotic use, and serious underlying illness. Until effective therapy is available, prevention of infection by proper infection control procedures and judicious antibiotic use is critical.

Anti-Bacterial Agents↗

Reducing the spread of antimicrobial-resistant microorganisms. Control of vancomycin-resistant enterococci.

Strategies to reduce the spread of hospital-acquired microorganisms resistant to multiple antimicrobial agents are discussed. Because hospitals have experienced a rapid increase in the incidence of infection and colonization with vancomycin-resistant enterococci (VRE) in the past 5 years, the Hospital Infection Control Practices Advisory Committee of the Centers for Disease Control and Prevention has issued recommendations for preventing the spread of vancomycin resistance. Controlling VRE dissemination in pediatric patients requires prompt detection of VRE by microbiology laboratories, education of staff and families about VRE, use of infection control measures to prevent person-to-person VRE transmission, and prudent vancomycin use.

Child↗

Antibiotic sensitivities of enterococci isolated from treated root canals.

Enterococci that persisted in debrided, medicated root canals were tested by the Kirby-Bauer procedure for sensitivity to various antibiotics. The 50 strains tested were uniformly sensitive to ampicillin and vancomycin. More than 90% were also sensitive to erythromycin. Varying degrees of sensitivity and resistance were noted to bacitracin, cephaloridine, cephalothin, chloramphenicol, gentamicin, and tetracycline. All organisms were either partly or wholly resistant to clindamycin; penicillin; streptomycin; and sulfadiazine, sulfamerazine, and sulfamethazine (triple sulfas).

Anti-Bacterial Agents↗

Epidemiology of colonisation of patients and environment with vancomycin-resistant enterococci.

BACKGROUND: Vancomycin-resistant enterococci (VRE) have emerged as nosocomial pathogens during the past 5 years, but little is known about the epidemiology of VRE. We investigated colonisation of patients and environmental contamination with VRE in an endemic setting to assess the importance of different sources of colonisation. METHODS: Between April 12, and May 29, 1995, cultures from body sites (rectum, groin, arm, oropharynx, trachea, and stomach) and from environmental surfaces (bedrails, drawsheet, blood-pressure cuff, urine containers, and enteral feed) were obtained daily from all newly admitted ventilated patients in our medical intensive-care unit (MICU). Rectal cultures were obtained from all non-ventilated patients in the MICU. Strain types of VRE were determined by pulsed-field gel electrophoresis. FINDINGS: There were 97 admissions of 92 patients, of whom 38 required mechanical ventilation. Colonisation with VRE on admission was more common in ventilated than in non-ventilated patients (nine [24%] vs three [6%], p < 0.05). Of the nine ventilated patients colonised with VRE on admission, one acquired a new strain of VRE in the MICU. Of the 29 ventilated patients who were not colonised with VRE on admission, 12 (41%) acquired VRE in the MICU. The median time to acquisition of VRE was 5 days (interquartile range 3-8). Of the 13 ventilated patients who acquired VRE, 11 (85%) were colonised with VRE by cross-colonisation. VRE were isolated from 157 (12%) of 1294 environmental cultures. The rooms of 13 patients were contaminated with VRE, but only three (23%) of these patients subsequently acquired colonisation with VRE. Pulsed-field gel electrophoresis of 262 isolates showed 20 unique strain types of VRE. INTERPRETATION: Frequent colonisation with VRE on MICU admission and subsequent cross-colonisation are important factors in the endemic spread of VRE. Persistent VRE colonisation in the gastrointestinal tract and on the skin, the presence of multiple-strain types of VRE, and environmental contamination may all contribute to the spread of VRE.

Adult↗

Methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci: therapeutic realities and possibilities.

During the past decade much effort has been devoted worldwide to limiting the spread of methicillin-resistant Staphylococcus aureus. However, the recent emergence of almost untreatable vancomycin-resistant enterococci has led to a new and unexpected public health problem in hospitals and the community. Moreover, the threat of transfer of glycopeptide resistance to S aureus means that development of alternative antimicrobial strategies has become urgent. Whereas major advances have been made in our understanding of methicillin and vancomycin resistance mechanisms, we still need to identify the sources and reservoirs of the genetic determinants of resistance and to discover how they disseminate in the environment. The outcome of the battle between antimicrobials and bacteria is still uncertain, but the challenge is worth meeting.

Anti-Bacterial Agents↗

Mechanisms of glycopeptide resistance in enterococci.

Inducible resistance to high levels of glycopeptide antibiotics in clinical isolates of enterococci is mediated by Tn1546 or related transposons. Tn1546 encodes the VanH dehydrogenase which reduces pyruvate to D-lactate (D-Lac) and the VanA ligase which catalyses synthesis of the depsipeptide D-alanyl-D-lactate (D-Ala-D-Lac). The depsipeptide replaces the dipeptide D-Ala-D-Ala leading to production of peptidoglycan precursors which bind glycopeptides with reduced affinity. In addition, Tn1546 encodes the VanX dipeptidase and the VanY D,D-carboxypeptidase that hydrolyse the dipeptide D-Ala-D-Ala and the C-terminal D-Ala residue of the cytoplasmic precursor UDP-MurNAC-L-Ala-gamma-D- Glu-L-Lys-D-Ala-D-Ala, respectively. These two proteins act in series to eliminate D-Ala-D-Ala-containing precursors. VanX is required for resistance whereas VanY only slightly increases the level of resistance mediated by VanH, VanA and VanX.

Amino Acid Sequence↗