Ana P Tedim1,2,3, Patricia Ruíz-Garbajosa1,2,4, Maria Concepción Rodríguez1, Mercedes Rodríguez-Baños1, Val F Lanza1,2,3, Laura Derdoy5, Gonzalo Cárdenas Zurita6, Elena Loza1, Rafael Cantón1,4, Fernando Baquero1,2,3, Teresa M Coque7,2,3. 1. Microbiology Department, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, Spain. 2. Unidad de Resistencia a Antibióticos y Virulencia Bacteriana asociada al Consejo Superior de Investigaciones Científicas (CSIC), Madrid, Spain. 3. Centros de Investigación Biomédica en Red de Epidemiología y Salud Pública (CIBER-ESP), Barcelona, Spain. 4. Spanish Network for Research in Infectious Diseases (REIPI), Seville, Spain. 5. Microbiology Department, Laboratory Division, Hospital General de Agudos Ramos Mejía, Ciudad Autónoma de Buenos Aires, Argentina. 6. Clinical Laboratory, Microbiology and Infectious Diseases Department, Clinica San Francisco, Quito, Ecuador. 7. Microbiology Department, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, Spain mariateresa.coque@salud.madrid.org teresacoque@gmail.com.
Abstract
OBJECTIVES: To investigate the population structure of Enterococcus faecium causing bloodstream infections (BSIs) in a tertiary Spanish hospital with low glycopeptide resistance, and to enhance our knowledge of the dynamics of emergence and spread of high-risk clonal complexes. METHODS: All available E. faecium causing BSIs (n = 413) in our hospital (January 1995-May 2015) were analysed for antibiotic susceptibility (CLSI), putative virulence traits (PCR, esp, hylEfm) and clonal relationship (SmaI-PFGE, MLST evaluated by goeBURST and BAPS). RESULTS: The increased incidence of BSIs caused by enterococci [2.3‰ of attended patients (inpatients and outpatients) in 1996 to 3.0‰ in 2014] significantly correlated with the increase in BSIs caused by E. faecium (0.33‰ of attended patients in 1996 to 1.3‰ in 2014). The BSIs Enterococcus faecalis:E. faecium ratio changed from 5:1 in 1996 to 1:1 in 2014. During the last decade an increase in E. faecium BSIs episodes in cancer patients (10.9% in 1995-2005 and 37.1% in 2006-15) was detected. Ampicillin-susceptible E. faecium (ASEfm; different STs/BAPS) and ampicillin-resistant E. faecium (AREfm; ST18/ST17-BAPS 3.3a) isolates were recovered throughout the study. Successive waves of BAPS 2.1a-AREfm (ST117, ST203 and ST80) partially replaced ASEfm and ST18-AREfm since 2006. CONCLUSIONS: Different AREfm clones (belonging to BAPS 2.1a and BAPS 3.3a) consistently isolated during the last decade from BSIs might be explained by a continuous and dense colonization (favouring both invasion and cross-transmission) of hospitalized patients. High-density colonization by these clones is probably enhanced in elderly patients by heavy and prolonged antibiotic exposure, particularly in oncological patients.
OBJECTIVES: To investigate the population structure of Enterococcus faecium causing bloodstream infections (BSIs) in a tertiary Spanish hospital with low glycopeptide resistance, and to enhance our knowledge of the dynamics of emergence and spread of high-risk clonal complexes. METHODS: All available E. faecium causing BSIs (n = 413) in our hospital (January 1995-May 2015) were analysed for antibiotic susceptibility (CLSI), putative virulence traits (PCR, esp, hylEfm) and clonal relationship (SmaI-PFGE, MLST evaluated by goeBURST and BAPS). RESULTS: The increased incidence of BSIs caused by enterococci [2.3‰ of attended patients (inpatients and outpatients) in 1996 to 3.0‰ in 2014] significantly correlated with the increase in BSIs caused by E. faecium (0.33‰ of attended patients in 1996 to 1.3‰ in 2014). The BSIs Enterococcus faecalis:E. faecium ratio changed from 5:1 in 1996 to 1:1 in 2014. During the last decade an increase in E. faecium BSIs episodes in cancerpatients (10.9% in 1995-2005 and 37.1% in 2006-15) was detected. Ampicillin-susceptible E. faecium (ASEfm; different STs/BAPS) and ampicillin-resistant E. faecium (AREfm; ST18/ST17-BAPS 3.3a) isolates were recovered throughout the study. Successive waves of BAPS 2.1a-AREfm (ST117, ST203 and ST80) partially replaced ASEfm and ST18-AREfm since 2006. CONCLUSIONS: Different AREfm clones (belonging to BAPS 2.1a and BAPS 3.3a) consistently isolated during the last decade from BSIs might be explained by a continuous and dense colonization (favouring both invasion and cross-transmission) of hospitalized patients. High-density colonization by these clones is probably enhanced in elderly patients by heavy and prolonged antibiotic exposure, particularly in oncological patients.
Authors: Bárbara Duarte; Ana P Pereira; Ana R Freitas; Teresa M Coque; Anette M Hammerum; Henrik Hasman; Patrícia Antunes; Luísa Peixe; Carla Novais Journal: Appl Environ Microbiol Date: 2019-11-14 Impact factor: 4.792
Authors: Ana P Tedim; Val F Lanza; Marina Manrique; Eduardo Pareja; Patricia Ruiz-Garbajosa; Rafael Cantón; Fernando Baquero; Teresa M Coque; Raquel Tobes Journal: Genome Announc Date: 2017-03-30
Authors: Andrew A Mahony; Andrew H Buultjens; Susan A Ballard; Elizabeth A Grabsch; Shirley Xie; Torsten Seemann; Rhonda L Stuart; Despina Kotsanas; Allen Cheng; Helen Heffernan; Sally A Roberts; Geoffrey W Coombs; Narin Bak; John K Ferguson; Glen C Carter; Benjamin P Howden; Timothy P Stinear; Paul D R Johnson Journal: Antimicrob Resist Infect Control Date: 2018-03-22 Impact factor: 4.887
Authors: Anna Weber; Friederike Maechler; Frank Schwab; Petra Gastmeier; Axel Kola Journal: Antimicrob Resist Infect Control Date: 2020-07-16 Impact factor: 4.887
Authors: Celia M Schell; Ana P Tedim; Mercedes Rodríguez-Baños; Mónica D Sparo; Sabina Lissarrague; Juan A Basualdo; Teresa M Coque Journal: Pathogens Date: 2020-02-20
Authors: Scott J Dos Santos; Zahra Pakzad; Chelsea N Elwood; Arianne Y K Albert; Soren Gantt; Amee R Manges; Tim J Dumonceaux; Evelyn J Maan; Janet E Hill; Deborah M Money Journal: Microbiol Spectr Date: 2021-09-29