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1. A review of current treatment strategies for infective endocarditis

Author

Ines Lakbar, David Luque Paz, Pierre Tattevin, CHU Pontchaillou [Rennes], CHU Toulouse [Toulouse], ARN régulateurs bactériens et médecine (BRM), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), This paper was not funded., Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), and Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )

Subjects
0301 basic medicine, Microbiology (medical), Oral treatment, medicine.medical_specialty, Prosthesis-Related Infections, Time Factors, empirical treatment, medicine.drug_class, [SDV]Life Sciences [q-bio], 030106 microbiology, Antibiotics, Heart Valve Diseases, review, Microbiology, antibiotics, 03 medical and health sciences, 0302 clinical medicine, enterococci, Virology, medicine, Endocarditis, Animals, Humans, 030212 general & internal medicine, Intensive care medicine, staphylococci, treatment, business.industry, HACEK, oral treatment, Endocarditis, Bacterial, medicine.disease, 3. Good health, Anti-Bacterial Agents, Empirical treatment, Infectious Diseases, streptococci, Infective endocarditis, Heart Valve Prosthesis, Treatment strategy, business
Abstract

International audience; Introduction Infective endocarditis is one of the most difficult-to-treat infectious diseases. Areas covered We restricted this review to the anti-infective treatment of the main bacteria responsible for infective endocarditis, i.e. staphylococci, streptococci, enterococci, and Gram-negative bacilli, including HACEK. Specific topics of major interest in treatment strategy are covered as well, including empirical treatment, oral switch, and treatment duration. We searched in the MEDLINE database to identify relevant studies, trials, reviews, or meta-analyses until May 2020. Expert opinion The use of aminoglycosides for the treatment of endocarditis has been dramatically reduced over the last 20 years. It should be administered once daily, and no longer than 2 weeks. For staphylococcal endocarditis, recent data reinforced the role of anti-staphylococcal penicillins, for methicillin-susceptible isolates (alternative, cefazolin), and vancomycin for methicillin-resistant isolates (alternative, daptomycin). For staphylococcal prosthetic-valve endocarditis, these treatments will be reinforced by the addition of gentamicin during the first 2 weeks, and rifampin throughout the whole treatment duration, i.e. 6 weeks. The optimal duration of antibacterial treatment is 4 weeks for most native valve endocarditis, and 6 weeks for prosthetic-valve endocarditis. The oral switch is safe in patients stabilized after the initial intravenous course.

Published
2021

2. β-lactam antibiotics promote bacterial mutagenesis via an RpoS-mediated reduction in replication fidelity

Author

Jörg Vogel, Ivan Matic, S. Crussard, Jesús Blázquez, Luisa Laureti, Zeynep Baharoglu, Didier Mazel, F. Darfeuille, Alexandro Rodríguez-Rojas, Arnaud Gutierrez, Heni Abida, Robustesse et évolvabilité de la vie (U1001), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Departamento de Biotecnología Microbiana, Centro Nacional de Biotecnología [Madrid] (CNB-CSIC), Consejo Superior de Investigaciones Científicas [Madrid] (CSIC)-Consejo Superior de Investigaciones Científicas [Madrid] (CSIC), Plasticité du Génome Bactérien - Bacterial Genome Plasticity (PGB), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Régulations Naturelles et Artificielles (ARNA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Bordeaux Ségalen [Bordeaux 2], Julius-Maximilians-Universität Würzburg (JMU), This work was supported by the FP7-HEALTH-F3-2010-241476 and ANR-09-BLAN-0251 grants. A.G. was supported by a fellowship from the French Ministry of Science and Education. D.M. was supported by the Institut Pasteur, Centre National de la Recherche Scientifique (CNRS-UMR 3525), the French National Research Agency (ANR-08-MIE-016), LABEX IBEID and the European Union Seventh Framework Programme EvoTAR. Z.B. was supported by a postdoctoral fellowship from the DIM Malinf. J.B. was supported by grants PI10/00105 (FIS) and REIPI (RD06/0008), both from Ministerio de Ciencia e Innovacion, Instituto de Salud Carlos III., We thank Dan Andersson’s lab (Uppsala University, Sweden) for providing the anti-DinB antibody, Marie Francoise Norel (Pasteur Institute, Paris) for providing the anti-RpoS antibody and Paul Modrich’s lab for providing the anti-MutS antibody., I.M., A.G., D.M., J.B., F.D. and J.V. designed the research and wrote the paper. A.G., L.L., H.A. and S.C. performed experiments with E. coli. Z.B. performed experiments and analysed data with V. cholerae. A.R.R. performed experiments and analysed data with P. aeruginosa. F.D. and J.V. performed in vitro experiments with SdsR and analysed data., ANR-09-BLAN-0251,bactadapt(2009), ANR-08-MIEN-0016,IIRE,Integrase d'integron recombinaison et expression(2008), European Project: 241476,EC:FP7:HEALTH,FP7-HEALTH-2009-single-stage,PAR(2010), European Project: 282004,EC:FP7:HEALTH,FP7-HEALTH-2011-single-stage,EVOTAR(2011), HOFFMANN, Isabelle, Blanc - - bactadapt2009 - ANR-09-BLAN-0251 - Blanc - VALID, Maladies Infectieuses et environnement - Integrase d'integron recombinaison et expression - - IIRE2008 - ANR-08-MIEN-0016 - MIE - VALID, Predicting antibiotic resistance - PAR - - EC:FP7:HEALTH2010-04-01 - 2013-03-31 - 241476 - VALID, Evolution and Transfer of Antibiotic Resistance - EVOTAR - - EC:FP7:HEALTH2011-10-01 - 2015-09-30 - 282004 - VALID, Centro Nacional de Biotecnologia, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), and Julius-Maximilians-Universität Würzburg [Wurtzbourg, Allemagne] (JMU)

Subjects
DNA Replication, medicine.drug_class, [SDV]Life Sciences [q-bio], Antibiotics, General Physics and Astronomy, Sigma Factor, MESH: DNA Replication, Biology, beta-Lactams, medicine.disease_cause, General Biochemistry, Genetics and Molecular Biology, Microbiology, 03 medical and health sciences, Antibiotic resistance, Bacterial Proteins, MESH: beta-Lactams, MESH: Anti-Bacterial Agents, Escherichia coli, medicine, Vibrio cholerae, MESH: Bacterial Proteins, 030304 developmental biology, MESH: Mutagenesis, 0303 health sciences, Multidisciplinary, Bacteria, 030306 microbiology, Pseudomonas aeruginosa, MESH: Escherichia coli, Mutagenesis, MESH: Reactive Oxygen Species, MESH: Sigma Factor, General Chemistry, biochemical phenomena, metabolism, and nutrition, Anti-Bacterial Agents, 3. Good health, [SDV] Life Sciences [q-bio], MESH: Bacteria, Regulon, MESH: Pseudomonas aeruginosa, bacteria, Reactive Oxygen Species, rpoS, MESH: Vibrio cholerae
Abstract

Antimicrobials: mismatch excels when ampicillin runs low. [Nat Rev Microbiol. 2013]; International audience; Regardless of their targets and modes of action, subinhibitory concentrations of antibiotics can have an impact on cell physiology and trigger a large variety of cellular responses in different bacterial species. Subinhibitory concentrations of β-lactam antibiotics cause reactive oxygen species production and induce PolIV-dependent mutagenesis in Escherichia coli. Here we show that subinhibitory concentrations of β-lactam antibiotics induce the RpoS regulon. RpoS regulon induction is required for PolIV-dependent mutagenesis because it diminishes the control of DNA-replication fidelity by depleting MutS in E. coli, Vibrio cholerae and Pseudomonas aeruginosa. We also show that in E. coli, the reduction in mismatch-repair activity is mediated by SdsR, the RpoS-controlled small RNA. In summary, we show that mutagenesis induced by subinhibitory concentrations of antibiotics is a genetically controlled process. Because this mutagenesis can generate mutations conferring antibiotic resistance, it should be taken into consideration for the development of more efficient antimicrobial therapeutic strategies.

Published
2013