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PubMed2000

Eradication of vancomycin resistant Enterococcus faecium from a paediatric oncology unit and prevalence of colonization in hospitalized and community-based children.

We previously reported an outbreak of vancomycin resistant enterococci (VRE) in a paediatric oncology unit in December 1995 which was associated with widespread environmental contamination of the unit with VRE. We undertook this study to evaluate the effectiveness of the infection control policy instituted subsequent to the outbreak and to investigate the underlying prevalence of VRE colonization in hospitalized, outpatient and community-based children. We sought to establish the molecular similarity of VRE isolates from the study. Stool specimens were obtained from outpatients at risk of VRE, hospital inpatients and from healthy community-based children. VRE colonization was eradicated from the inpatient unit within 11 months, but in outpatients, 16 months after the outbreak, 4 of 137 (2.9 %) attending oncology outpatients, 5 of 65 (7.7%) with cystic fibrosis and 1 of 12 (8.3 %) with liver disease were found to be colonized with VRE. The isolates were all Enterococcus faecium, Van A phenotype except one E. casseliflavus of the Van C phenotype. All were unique in SmaI DNA macrorestriction patterns with the exception of two isolates, which were similar to the original outbreak strain and three further isolates of a single strain but which differed from the outbreak strain. Of 315 hospital inpatients, 2.5 % were colonized with VRE of the Van C resistance phenotype but VRE was not detected in 116 healthy, community-based children. We conclude that effective strategies can successfully control spread of VRE but despite a low prevalence of VRE colonization in hospital patients and in community-based children, outbreaks can occur when infection control practices are not optimal. Continued vigilance to detect VRE and limit spread within hospitals is therefore necessary.

Adolescent↗
PubMed1991

Tetracycline resistance heterogeneity in Enterococcus faecium.

The tetracycline (Tet) determinants, which encode resistance either to tetracyclines without minocycline (Tcr) or to tetracyclines including minocycline (Tcr-Mnr), of 30 wild-type clinical isolates of Enterococcus faecium were identified and localized. The Tet determinants were transferred by conjugation into a plasmid-free Enterococcus faecalis recipient at frequencies of 10(-6) to 10(-9) transconjugants per donor, as follows: Tcr, 6 strains; Tcr-Mnr, 14 strains; both Tcr and Tcr-Mnr, 6 strains; no detectable transfer, 4 strains. Classes L (Tcr phenotype) and M and O (Tcr-Mnr phenotype) of the Tet determinants were identified by DNA-DNA hybridization experiments. The Tet L determinant was plasmid-borne in 18 strains and was chromosomal in 2 strains. Tet M was chromosomal in 27 strains and plasmid-borne (pIP1534) in 1 strain; pIP1534 also carried Tet L. Tet M was located on Tn916-like elements in 22 strains and on a Tn916-modified element in 1 strain. Tet O was detected in only one strain in which it was plasmid-borne. Both Tet L and Tet M determinants were carried by 19 strains. One strain carried, in addition to chromosomal nonconjugative Tet L and Tet M determinants, a conjugative Tcr-Mnr marker which did not correspond to any Tet determinant tested in this study. These results attest to the genetic complexity of tetracycline resistance in E. faecium strains.

Chromosomes, Bacterial↗
PubMed1990

Bactericidal activity of vancomycin, daptomycin, ampicillin and aminoglycosides against vancomycin-resistant Enterococcus faecium.

Daptomycin, vancomycin, ampicillin and aminoglycosides, alone or in combination, were tested for their bactericidal activity against 15 isolates of vancomycin-resistant Enterococcus faecium from immunocompromised children. The kill-kinetic studies at clinically achievable concentrations demonstrated that daptomycin alone or in combination with ampicillin had the greatest bactericidal activity.

Aminoglycosides↗
PubMed1997

Colonization with vancomycin-resistant Enterococcus faecium: comparison of a long-term-care unit with an acute-care hospital.

OBJECTIVE: To compare the epidemiology of vancomycin-resistant Enterococcus faecium (VRE) in a long-term-care unit and an acute-care hospital. DESIGN: Point-prevalence surveys for VRE rectal colonization of patients were carried out over a 21-month period in patients in a long-term-care unit and an acute-care hospital (medical ward and intensive-care units). The environment and hands of healthcare workers also were sampled for VRE. Contour-clamped homogeneous electric field (CHEF) electrophoresis was used to evaluate possible transmission among roommates and the relatedness of patient strains to those in the environment and on the hands of healthcare workers. SETTING: A 200-bed Veterans Affairs Medical Center with an attached 90-bed long-term-care unit. RESULTS: From December 1994 to January 1996, rectal VRE colonization of patients in the long-term-care unit increased significantly from 9% to 22%. In contrast, patients on the medical ward rarely were colonized after the first survey in December 1994, and only two intensive-care-unit patients were found to be colonized during the four surveys. The environment was contaminated persistently in the long-term-care unit. In the four surveys, carriage of VRE on hands of healthcare workers varied from 13% to 41%; 65% of healthcare workers with VRE found on their hands worked in the long-term-care unit. Seven different strains were identified by CHEF typing. Although the initial survey found only vanA strains, subsequent surveys showed vanB strains also were present. CONCLUSIONS: Residents of a long-term-care unit frequently were colonized with VRE, but infections were uncommon in this population. The environment of the long-term-care unit was contaminated with VRE, and VRE was found frequently on the hands of healthcare workers in this unit. Both vanA and vanB genotypes were found in this setting.

Anti-Bacterial Agents↗
PubMed1987

Bacteriostatic and bactericidal activities of beta-lactams against Streptococcus (Enterococcus) faecium are associated with saturation of different penicillin-binding proteins.

The MICs and MBCs of benzylpenicillin, ampicillin, cefotaxime, and methicillin were evaluated against a Streptococcus (Enterococcus) faecium wild-type strain and against three mutants hyperproducing PBP 5 in cells incubated at both optimal and suboptimal temperatures. In the wild-type strain grown at optimal temperature, the MBCs of all beta-lactams were significantly greater than the MICs (bacteriostatic effect). As opposed to this, in the same cells grown at suboptimal temperature and in the mutants hyperproducing PBP 5 at all temperatures, the MICs of all antibiotics coincided with the MBCs (bactericidal effect). Under all conditions in which the MIC and MBC were the same, with all antibiotics, growth inhibition occurred only at the minimal concentration saturating all penicillin-binding proteins (PBPs) (or at higher concentrations). On the contrary, under conditions in which the MIC was lower than the MBC, only some of the PBPs were saturated (or bound) at both the MIC and the MBC, PBP 5 in no case being either saturated or bound. Under all conditions in which saturation of all PBPs was needed for growth inhibition, cells died at all antibiotic MBCs with kinetics which were much faster than those with which they died at the MBCs under conditions in which not all PBPs were saturated (or bound). In addition, under the former conditions, antibiotic concentrations above the MBCs did not significantly accelerate cell death kinetics, while under the latter conditions there was an acceleration in kinetics with increasing antibiotic concentrations up to full saturation of PBPs. It is suggested that the killing that occurs when all PBPs are saturated is a direct consequence of inactivation of PBP functions, while killing occurring when only some of them are saturated or bound is also (or mainly) an indirect consequence of inability of cells to grow and that, in S. faecium, the targets for growth inhibition and cell killing reside in different PBPs: for the latter effect, inactivation of one (or more) of the high-molecular-weight PBPs is sufficient, whereas in the former case inactivation of PBP 5 is necessary (after saturation of all other PBPs).

Anti-Bacterial Agents↗
PubMed2003

Comparison of the incidence of virulence determinants and antibiotic resistance between Enterococcus faecium strains of dairy, animal and clinical origin.

Enterococci are part of the dominant microbiota of several dairy products. They are also present in the gut of humans and animals. Their presence in traditional raw milk cheeses is probably due to faecal contamination of milk during milking. Due to their importance as a cause of nosocomial infections, enterococci are acquiring increased significance. Such infections are becoming more and more difficult to treat as resistance to antibiotics increases. The aim of this investigation was to compare the potential virulence of Enterococcus faecium isolated from different ecological habitats and to establish if strains isolated from dairy products should really be considered as potential pathogens. In the present work, the antibiotic resistance pattern of 40 E. faecium strains isolated from dairy products, 26 E. faecium isolated from ewes' faeces and 28 clinical isolates of the same species was studied, and checks were made to see if known virulence determinants were present. Resistance to 12 different antibiotics commonly used in the treatment of human infections was tested using the broth microdilution method as described by the NCCLS. In addition, polymerase chain reaction (PCR) tests were carried out to see if genes for vancomycin resistance were present. The presence of the aggregation substance (AS) gene, the surface protein gene esp, the accessory colonisation factor ace, the Enterococcus faecalis endocarditis antigen efaA and the gelatinase gelE gene, which are involved in the virulence of enterococci, were also tested by PCR. The results of this study clearly indicate that E. faecium strains isolated from both cheese and sheep faeces are less pathogenic than those isolated from clinical samples. A similar pattern of resistance to antibiotics was observed in both dairy and animal strains. It was also found that there was difference in the kind of virulence determinants present in dairy and clinical isolates, while no virulence traits were found in sheep faeces strains. The results of this study suggest that E. faecium from traditional Sardinian raw milk cheeses should not be considered to be the main source of untreatable nosocomial enterococcal infections in humans in the island of Sardinia.

Animals↗
PubMed2003

Peritoneal dialysis fluid concentrations of linezolid in the treatment of vancomycin-resistant Enterococcus faecium peritonitis.

OBJECTIVE: To determine linezolid concentrations in peritoneal dialysis fluid after multiple oral doses of the drug in a 46-year-old man with vancomycin-resistant Enterococcus faecium peritonitis who was undergoing peritoneal dialysis. METHODS: After administration of oral linezolid 600 mg twice/day was started, peritoneal dialysis fluid was collected at the end of several 4- and 8-hour dwell times and submitted for analysis of linezolid concentration. Before linezolid therapy was begun, and immediately after several peritoneal dialysis exchanges, 30 ml of expended peritoneal dialysis fluid was collected in a sterile container and immediately frozen at -70 degrees C until analysis by high-performance liquid chromatography. RESULTS: Peritoneal dialysis concentrations of linezolid greater than 4 microg/ml were achieved after the first dose of linezolid and maintained after repeated doses. During the course of therapy, mean linezolid concentrations in peritoneal dialysis fluid tended to increase (mean 7.60 pg/ml, range 3.54-16.2 microg/ml). All assayed peritoneal dialysis samples demonstrated linezolid concentrations greater than 4 microg/ml at the end of 4- or 8-hour dwell times, except for one level after a missed dose on linezolid treatment day 3. Duration of dwell times did not appear to correlate with linezolid concentrations. CONCLUSION: In this patient, linezolid 600 mg twice/day penetrated into peritoneal dialysis fluid at or above the concentrations necessary to treat common gram-positive bacteria. Linezolid therapy is likely to have a role in peritoneal dialysis-associated peritonitis based on its antimicrobial activity, pharmacokinetic properties, ease of administration, and tolerability.

Acetamides↗
PubMed1993

Antibiotic treatment of experimental endocarditis due to vancomycin- and ampicillin-resistant Enterococcus faecium.

We compared ciprofloxacin, rifampin, and gentamicin treatments, alone and in combination, for 5 days in the therapy of experimental aortic valve endocarditis in rats caused by a clinical isolate of vancomycin-resistant Enterococcus faecium. The MICs and MBCs of vancomycin, ciprofloxacin, rifampin, and gentamicin were 250 and > 1,000, 3.1 and 6.3, 0.098 and 1.6, and 12.5 and > 50 micrograms/ml, respectively. Infected rats were sacrificed after completing 5 days of therapy. Additional rats within each treatment group were followed for 5 days beyond the last dose of antibiotic therapy. Although survivals in the different groups were not significantly different after 5 days of therapy, survival was significantly better 5 days beyond the last dose of antibiotic therapy in rats treated with rifampin-containing regimens. The combination of ciprofloxacin and gentamicin was bactericidal in vitro and in vegetations from rats with enterococcal endocarditis. Rifampin alone was similarly bactericidal in vivo, but it was not significantly better than rifampin in combination with other antibiotics. Subpopulations resistant to rifampin, but not ciprofloxacin, were detected in the inoculum and in most vegetations during therapy. However, the combination of ciprofloxacin plus both gentamicin and rifampin reduced both the rifampin-susceptible and -resistant population in vegetations of 9 of 10 animals below the level of detection after 5 days of therapy. Nevertheless, a residual enterococcal population apparently remained in numbers of < 2 log10 CFU/g after 5 days of therapy, which resulted in relapse. Perhaps a longer course of therapy would have eliminated this residual population and improved efficacy.

Ampicillin Resistance↗
PubMedDate not supplied

[Role of Enterococcus faecium SF 68 in experimental infection in mice].

The normal intestinal flora is an important defence against various infectious agents. It also allows important metabolic stages in the host. The Authors studied the ability of Enterococcus faecium SF 68 to protect the mice (Swiss strain) from infection by Salmonella typhi and its role when used with penicillin in infection by Staphylococcus aureus. Our results showed that SF 68, determined a good protection against infection. Moreover the association E. faecium SF 68-antibiotic lowers the mortality rate in the infected mice compared with the control group.

Animals↗
PubMed1999

An interprovincial external quality assessment of the ability of Canadian laboratories to detect the vancomycin and penicillin resistance of Enterococcus faecium D366.

OBJECTIVE: To evaluate the ability of Canadian laboratories to identify enterococci and detect low-level resistance to penicillin, ampicillin and vancomycin in five provinces and two territories by two external quality assessment schemes. METHODS: Enterococcus faecium, strain D366, with minimum inhibitory concentrations for vancomycin and penicillin of 32 and 16 mg/L respectively, was distributed during a routine proficiency survey. Laboratories were required to culture and identify the isolate and to test antimicrobial susceptibility. Participants were assessed against consensus reference values. RESULTS: Three hundred and sixty-four hospital, commercial and public-health laboratories participated, using their established procedures for patient samples. The isolate was identified to the species level by 222 (61%) laboratories and to the genus level by a further 98 participants. Forty-four failed to meet the expected standard. Vancomycin resistance was detected by 94%. Those reporting a falsely susceptible result used disk diffusion testing. Penicillin resistance was noted by 250 of 258 laboratories reporting on this agent. An incorrect ampicillin-susceptible finding was reported by 62 of 147 laboratories using automated microdilution or agar dilution methods. CONCLUSIONS: Most laboratories identified the isolate to an appropriate level. Detection of low-level vancomycin and penicillin resistance was achieved by the majority. Ampicillin resistance was less readily detected.

Journal Article↗
PubMed1989

[A case report of meningitis and sepsis due to Enterococcus faecium complicated with strongyloidiasis].

A 80 year-old male was transferred to our department on 18th Aug. 1988, for high fever and clouding of the consciousness. He had been treated with steroid hormone (betamethasone 3.0 mg/day for 15 days) for his uveitis. Enterococcus faecium was isolated from both blood and spinal fluid, and then Strongyloides sterocoralis was revealed both in the sputum and stool. Anti-Human T-cell leukemia virus 1 (HTLV-1) antibody was also positive serologically. At first, beta-lactam antibiotics were used for the treatment of purulent meningitis and sepsis, but after performing sensitivity tests for E. faecium, the antibiotics were changed to rifampicin (RFP), fosfomycin (FOM) and ofloxacin (OFLX) for their excellent activity against the organism. After the clinical symptoms, subsided, thiabendazole was used for disseminated strongyloidiasis in daily doses of 2,500 mg for six days initially. The drug was used three times with two week intervals. Both bacterial and parasite infections subsided and no recurrence has been noticed until now. This is the first case of meningitis caused by E. facium complicated with strongyloidiasis.

Aged↗
PubMed2003

Comparative in vitro activity of linezolid and five other antimicrobials against nosocomial isolates of methicillin-resistant Staphylococcus aureus, methicillin-resistant Staphylococcus epidermidis and vancomycin-resistant Enterococcus faecium.

The activity of linezolid in comparison to vancomycin, teicoplanin, oxacillin, clindamycin and gentamicin was tested against 60 strains of methicillin-resistant Staphylococcus aureus, 60 strains of methicillin-resistant Staphylococcus epidermidis isolated from patients with nosocomial infections and 24 strains of vancomycin-resistant Enterococcus faecium isolated from feces of hospitalized patients. Minimum Inhibitory Concentrations (MICs) were determined by the Epsilometer test method. All tested strains were sensitive to linezolid and specifically all methicillin-resistant S. aureus had MIC range 0.25-3.00, MIC50 = 0.75, MIC90 = 1.5, all methicillin-resistant S. epidermidis had MIC range 0.125-1.5, MIC50 = 0.5, MIC90 = 1 and all vancomycin-resistant E. faecium had MIC range 0.5-1.5, MIC50 = 1, MIC90 = 1. Linezolid is the first of a novel antimicrobial class, the oxazolidinones, which is a promising treatment for serious Gram-positive infections, including multiresistant strains.

Acetamides↗
PubMed2002

Characterization of anti-Listeria monocytogenes bacteriocins from Enterococcus faecalis, Enterococcus faecium, and Lactococcus lactis strains isolated from Raïb, a Moroccan traditional fermented milk.

Seventy-four samples of raïb, a Moroccan traditional fermented milk, were screened for their anti-Listeria monocytogenes activity. Nine lactic acid bacteria with antilisterial activity were isolated and identified as Lactococcus lactis [4], Enterococcus faecium [4], and E. faecalis [1]. Antibacterial spectra, determined against 45 target strains, led to the selection of four antibacterial-producing strains, which were further characterized. Their anti-microbial agents, inactivated by one or more proteases, were designed as bacteriocins. Lactococcin R9/2 and R10/1 showed the broadest range of inhibitory action. Anti-bacterial spectra and physico-chemical properties suggest that these bacteriocins were similar to nisin. Enterocin R69 had a specificity of action against Listeria spp., whereas Enterocin R18 had a broad spectrum of activity. Lc. lactis R9/2 and E. faecalis R18 were able to coagulate sterilised UHT milk at 30 degrees C in 24 h and induced a 2 log reduction in L. monocytogenes ATCC 15313 population.

Animals↗
PubMed1990

Induction of vancomycin resistance in Enterococcus faecium by inhibition of transglycosylation.

Vancomycin resistance has recently been recognized among clinical isolates of enterococci. Resistance is inducible, and associated with production of a novel 39 kDa membrane protein. The mechanism by which exposure to vancomycin, which does not penetrate the cell membrane, induces resistance is unknown. In the vancomycin resistant strain Enterococcus faecium 228, resistance was also inducible by moenomycin, suggesting that inhibition of the transglycosylation step in peptidoglycan synthesis may be required for induction of resistance. Cytoplasmic pools of peptidoglycan precursors were increased after exposure to vancomycin or moenomycin, representing a potential means for regulation of induction.

Cytoplasm↗
PubMed2003

Occurrence and spread of antibiotic resistances in Enterococcus faecium.

Enterococci are the second to third most important bacterial genus in hospital infections. Especially Enterococcus (E.) faecium possesses a broad spectrum of natural and acquired antibiotic resistances which are presented in detail in this paper. From medical point of view, the transferable resistances to glycopeptides (e.g., vancomycin, VAN, or teicoplanin, TPL) and streptogramins (e.g., quinupristin/dalfopristin, Q/D) in enterococci are of special interest. The VanA type of enterococcal glycopeptide resistance is the most important one (VAN-r, TPL-r); its main reservoir is E. faecium. Glycopeptide-resistant E. faecium (GREF) can be found in hospitals and outside of them, namely in European commercial animal husbandry in which the glycopeptide avoparcin (AVO) was used as growth promoter in the past. There are identical types of the vanA gene clusters in enterococci from different ecological origins (faecal samples of animals, animal feed, patients in hospitals, persons in the community, waste water samples). Obviously, across the food chain (by GREF-contaminated meat products), these multiple-resistant bacteria or their vanA gene clusters can reach humans. In hospital infections, widespread epidemic-virulent E. faecium isolates of the same clone with or without glycopeptide resistance can occur; these strains often harbour different plasmids and the esp gene. This indicates that hospital-adapted epidemic-virulent E. faecium strains have picked up the vanA gene cluster after they were already widely spread. The streptogramin virginiamycin was also used as feed additive in commercial animal husbandry in Europe for more than 20 years, and it created reservoirs for streptogramin-resistant E. faecium (SREF). In 1998/1999, SREF could be isolated in Germany from waste water of sewage treatment plants, from faecal samples and meat products of animals that were fed virginiamycin (cross resistance to Q/D), from stools of humans in the community, and from clinical samples. These isolations of SREF occurred in a time before the streptogramin combination Q/D was introduced for therapeutic purposes in German hospitals in May 2000, while other streptogramins were not used in German clinics. This seems to indicate that the origin of these SREF or their streptogramin resistance gene(s) originated from other sources outside the hospitals, probably from commercial animal husbandry. In order to prevent the dissemination of multiple antibiotic-resistant enterococci or their transferable resistance genes, a prudent use of antibiotics is necessary in human and veterinary medicine, and in animal husbandry.

Animal Husbandry↗
PubMed1999

From vanA Enterococcus hirae to vanA Enterococcus faecium: a study of feed supplementation with avoparcin and tylosin in young chickens.

Fifteen newborn chickens were isolated in separate cages after 1 month of living together, divided into three groups, and challenged for 5 weeks with seed food which either was supplemented with avoparcin (10 mg/kg of animal food) or tylosin (40 mg/kg) or was nonsupplemented. At 9 weeks of age and after the 5-week challenge, all chickens received nonsupplemented feed for 4 additional weeks. At 4, 9, and 13 weeks of life, feces were collected and inoculated on M-Enterococcus agar plates with and without vancomycin (4 micrograms/ml). vanA-containing Enterococcus hirae was isolated from 11 of 15 chickens before antibiotic challenge, without detection of vancomycin-resistant Enterococcus faecium. At 9 weeks of age and after the 5-week avoparcin challenge, vanA E. hirae strains were no longer detected, but five of five chickens now had vanA E. faecium. At a lower frequency, vanA E. faecium had also displaced vanA E. hirae in both the tylosin group (one of four chickens) and the control group (two of five chickens). One month after avoparcin discontinuation, the number of chickens colonized with vanA E. faecium decreased from five to one. All vanA-containing E. hirae strains detected in the first month of life and most of the vanA-containing E. faecium strains detected in the second month of life showed identical ApaI and SmaI restriction patterns, respectively, when analyzed by pulsed-field gel electrophoresis. All vanA E. hirae isolates transferred glycopeptide and macrolide resistance to Enterococcus faecalis JH2-2 in vitro; the level of glycopeptide resistance was higher in the transconjugants than in the donor E. hirae strains. These data suggest that E. hirae may be a significant source of vanA determinants with the potential of transfer to other enterococcal species from humans or animals.

Animals↗
PubMed2000

Comparison of antimicrobial resistance phenotypes and resistance genes in Enterococcus faecalis and Enterococcus faecium from humans in the community, broilers, and pigs in Denmark.

Enterococcus faecalis and E. faecium isolated from humans in the community (98 and 65 isolates), broilers (126 and 122), and pigs (102 and 88) during 1998 were tested for susceptibility to 12 different antimicrobial agents and for the presence of selected genes encoding resistance using PCR. Furthermore, the presence of vancomycin resistant enterococci was examined in 38 human stool samples using selective enrichment. Widespread resistance to chloramphenicol, macrolides, kanamycin, streptomycin, and tetracycline was found among isolates from all three sources. All E. faecium isolates from humans and pigs were susceptible to avilamycin, whereas 35% of isolates from broilers were resistant. All E. faecium isolates from humans were susceptible to vancomycin, whereas 10% and 17% of isolates from broilers and pigs, respectively, were resistant. A vancomycin resistant E. faecium isolate was found in one of the 38 human fecal samples examined using selective enrichment. All vancomycin resistant isolates contained the vanA gene, all chloramphenicol resistant isolates the cat(pIP501) gene, and all five gentamicin resistant isolates the aac6-aph2 gene. Sixty-one (85%) of 72 erythromycin resistant E. faecalis examined and 57 (90%) of 63 erythromycin resistant E. faecium isolates examined contained ermB. Forty (91%) of the kanamycin resistant E. faecalis and 18 (72%) of the kanamycin resistant E. faecium isolates contained aphA3. The tet(M) gene was found in 95% of the tetracycline resistant E. faecalis and E. faecium isolates of human and animal origin, examined. tet(K) was not observed, whereas tet(L) was detected in 17% of tetracycline resistant E. faecalis isolates and in 16% of the E. faecium isolates. tet(O) was not detected in any of the isolates from pigs, but was observed in 38% of E. faecalis isolates from broilers, in two E. faecalis isolates from humans and in three E. faecium isolates from broilers. tet(S) was not detected among isolates from animals, but was observed in 31% of E. faecalis and one E. faecium isolate from humans. This study showed a frequent occurrence of antimicrobial resistance and the presence of selected resistance genes in E. faecalis and E. faecium isolated from humans, broilers and pigs. Differences in the occurrence of resistance and tetracycline resistance genes were observed among isolates from the different sources. However, similar resistance patterns and resistance genes were detected frequently indicating that transmission of resistant enterococci or resistance genes takes place between humans, broilers, and pigs.

Animals↗