Dataset Information

Epidemiology of Vancomycin-Resistant Enterococcus faecium and Enterococcus faecalis Colonization in Nursing Facilities.

ABSTRACT: Background:Vancomycin-resistant Enterococcus faecium and Enterococcus faecalis frequently colonize nursing facility (NF) residents, creating opportunities for vancomycin-resistant Enterococcus (VRE) transmission and dissemination of mobile genetic elements conferring antimicrobial resistance. Most VRE studies do not speciate; our study addresses this lack and compares the epidemiology of E faecium and E faecalis. Methods:We enrolled 651 newly admitted patients from 6 different NFs and collected swabs from several body sites at enrollment, 14 days, 30 days, and monthly thereafter for up to 6 months. The VRE were speciated using a duplex polymerase chain reaction. We used multinomial logistic regression models to compare risk factors associated with colonization of E faecium and E faecalis. Results:Overall, 40.7% were colonized with E faecium, E faecalis, or both. At enrollment, more participants were colonized with E faecium (17.8%) than E faecalis (8.4%); 3.2% carried both species. Enterococcus faecium was carried twice as long as E faecalis (69 days and 32 days, respectively), but incidence rates were similar (E faecium, 3.9/1000 person-days vs E faecalis, 4.1/1000 person-days). Length of stay did not differ by species among incident cases. Residents who used antibiotics within the past 30 days had a greater incidence of both E faecium (odds ratio [OR]?=?2.89; 95% confidence interval [CI], 1.82-4.60) and E faecalis (OR?=?1.80; 95% CI, 1.16-2.80); device use was most strongly associated with the incidence of E faecium colonization (OR?=?2.01; 95% CI, 1.15-3.50). Conclusions:Recent increases in vancomycin-resistant E faecium prevalence may reflect increased device use and longer duration of carriage.

SUBMITTER: Davis E

PROVIDER: S-EPMC6979485 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Epidemiology of Vancomycin-Resistant <i>Enterococcus faecium</i> and <i>Enterococcus faecalis</i> Colonization in Nursing Facilities.

Davis Elyse E Hicks Liam L Ali Ihsan I Salzman Elizabeth E Wang Joyce J Snitkin Evan E Gibson Kristen K Cassone Marco M Mody Lona L Foxman Betsy B

Open forum infectious diseases 20200106 1

<h4>Background</h4>Vancomycin-resistant <i>Enterococcus faecium</i> and <i>Enterococcus faecalis</i> frequently colonize nursing facility (NF) residents, creating opportunities for vancomycin-resistant <i>Enterococcus</i> (VRE) transmission and dissemination of mobile genetic elements conferring antimicrobial resistance. Most VRE studies do not speciate; our study addresses this lack and compares the epidemiology of <i>E faecium</i> and <i>E faecalis</i>.<h4>Methods</h4>We enrolled 651 newly adm ...[more]

PMID: 31993459

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Project description:Enterococcus faecium clinical isolates A902 and BM4538, which were resistant to relatively high levels of vancomycin (128 and 64 microg/ml, respectively) and to low levels of teicoplanin (4 microg/ml), and Enterococcus faecalis clinical isolates BM4539 and BM4540, which were resistant to moderate levels of vancomycin (16 microg/ml) and susceptible to teicoplanin (0.25 microg/ml), were studied. They were constitutively resistant by synthesis of peptidoglycan precursors ending with d-alanyl-d-lactate and harbored a chromosomal vanD gene cluster which was not transferable by conjugation to other enterococci. VanX(D) activity, which is not required in the absence of d-Ala-d-Ala, was low in the four strains, although none of the conserved residues was mutated; and the constitutive VanY(D) activity in the membrane fractions was inhibited by penicillin G. The mutations E(13)G in the region of d-alanine:d-alanine ligase (which is implicated in d-Ala1 binding in A902) and S(319)N of the serine involved in ATP binding in BM4538 and a 7-bp insertion at different locations in BM4539 and BM4540 (which led to putative truncated proteins) led to the production of an impaired enzyme and accounted for the lack of d-Ala-d-Ala-containing peptidoglycan precursors. The same 7-bp insertion in vanS(D) of BM4539 and BM4540 and a 1-bp deletion in vanS(D) of A902, which in each case led to a putative truncated and presumably nonfunctional protein, could account for the constitutive resistance. Strain BM4538, with a functional VanS(D), had a G(140)E mutation in VanR(D) that could be responsible for constitutive glycopeptide resistance. This would represent the first example of constitutive van gene expression due to a mutation in the structural gene for a VanR transcriptional activator. Study of these four additional strains that could be distinguished on the basis of their various assortments of mutations confirmed that all VanD-type strains isolated so far have mutations in the ddl housekeeping gene and in the acquired vanS(D) or vanR(D) gene that lead to constitutive resistance to vancomycin.

Project description:We studied the clinical isolates Enterococcus faecium NEF1, resistant to high levels of vancomycin (MIC, 512 microg/ml) and teicoplanin (MIC, 64 microg/ml); Enterococcus faecium BM4653 and BM4656 and Enterococcus avium BM4655, resistant to moderate levels of vancomycin (MIC, 32 microg/ml) and to low levels of teicoplanin (MIC, 4 microg/ml); and Enterococcus faecalis BM4654, moderately resistant to vancomycin (MIC, 16 microg/ml) but susceptible to teicoplanin (MIC, 0.5 microg/ml). The strains were distinct, were constitutively resistant via the synthesis of peptidoglycan precursors ending in D-alanyl-D-lactate, and harbored a chromosomal vanD gene cluster that was not transferable. New mutations were found in conserved domains of VanS(D): at T(170)I near the phosphorylation site in NEF1, at V(67)A at the membrane surface in BM4653, at G(340)S in the G2 ATP-binding domain in BM4655, in the F domain in BM4656 (a 6-bp insertion), and in the G1 and G2 domains of BM4654 (three mutations). The mutations resulted in constitutivity, presumably through the loss of the phosphatase activity of the sensor. The chromosomal Ddl D-Ala:D-Ala ligase had an IS19 copy in NEF1, a mutation in the serine (S(185)F) or near the arginine (T(289)P) involved in D-Ala1 binding in BM4653 or BM4655, respectively, and a mutation next to the lysine (P(180)S) involved in D-Ala2 binding in BM4654, leading to the production of an impaired enzyme. In BM4653 vanY(D), a new insertion sequence, ISEfa9, belonging to the IS3 family, resulted in the absence of D,D-carboxypeptidase activity. Strain BM4656 had a functional D-Ala:D-Ala ligase, associated with high levels of both VanX(D) and VanY(D) activities, and is the first example of a VanD-type strain with a functional Ddl enzyme. Study of these five clinical isolates, displaying various assortments of mutations, confirms that all VanD-type strains isolated so far have undergone mutations in the vanS(D) or vanR(D) gene, leading to constitutive resistance, but that the Ddl host ligase is not always impaired. Based on sequence differences, the vanD gene clusters could be assigned to two subtypes: vanD-1 and vanD-4.

Dataset Information

Epidemiology of Vancomycin-Resistant Enterococcus faecium and Enterococcus faecalis Colonization in Nursing Facilities.

Publications

Epidemiology of Vancomycin-Resistant <i>Enterococcus faecium</i> and <i>Enterococcus faecalis</i> Colonization in Nursing Facilities.

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