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1. Clinically applicable irreversible electroporation for eradication of micro-organisms.

Author

Korem M, Goldberg NS, Cahan A, Cohen MJ, Nissenbaum I, and Moses AE

Subjects
Anti-Bacterial Agents pharmacology, Colony Count, Microbial, Humans, Oxacillin pharmacology, Candida albicans growth & development, Cell Membrane pathology, Electroporation methods, Escherichia coli growth & development, Pseudomonas aeruginosa growth & development, Staphylococcus aureus growth & development, Streptococcus pyogenes growth & development
Abstract

Irreversible electroporation (IRE) damages cell membranes and is used in medicine for nonthermal ablation of malignant tumours. Our aim was to evaluate the antimicrobial effect of IRE. The pathogenic micro-organisms, Staphylococcus aureus, Streptococcus pyogenes, Escherichia coli, Pseudomonas aeruginosa and Candida albicans were subjected to IRE. Survival was measured as a function of voltage and the number of pulses applied. Combined use of IRE and oxacillin for eradication of Staph. aureus was also tested. Log10 reduction in micro-organisms positively correlated with the number of applied pulses. The colony count of Strep. pyogenes and E. coli declined by 3·38 and 3·05 orders of magnitude, respectively, using an electric field of 2000 V and 100 pulses. Killing of Staph. aureus and P. aeruginosa was achieved with a double cycle of IRE (2000, 1500 V and repeated 1250 V respectively) of 50-100 IRE pulses. The addition of subclinical inhibitory concentrations of oxacillin to the Staph. aureus suspension prior to IRE led to total bacterial death, demonstrating synergism between oxacillin and IRE. Our results demonstrate that using IRE with clinically established parameters has a marked in vitro effect on pathogenic micro-organisms and highlights the potential of IRE as a treatment modality for deep-seated infections, particularly when combined with low doses of antibiotics., Significance and Impact of the Study: Irreversible electroporation (IRE) is utilized in interventional radiology to treat cancer patients. In this study we evaluated in vitro the antimicrobial effect of IRE. We demonstrated that using IRE with clinically established parameters has a marked effect on pathogenic micro-organisms and is synergistic to antimicrobials when both are combined. Our results point to the potential of IRE as a treatment modality for deep-seated infections., (© 2018 The Society for Applied Microbiology.)

Published
2018
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2. Global gene expression in Staphylococcus aureus following exposure to alcohol.

Author

Korem M, Gov Y, and Rosenberg M

Subjects
Acetaldehyde metabolism, Alcohol Dehydrogenase genetics, Alcohol Dehydrogenase metabolism, Amino Acids metabolism, Bacterial Proteins genetics, Bacterial Proteins metabolism, Biofilms drug effects, Biofilms growth & development, Cell Line, Ethanol metabolism, Gene Expression Profiling, Hemolysin Proteins genetics, Hemolysin Proteins metabolism, Hemolysis, Humans, Hydrogen-Ion Concentration, Keratinocytes cytology, Keratinocytes physiology, Oligonucleotide Array Sequence Analysis, Oxidation-Reduction, Oxidative Stress drug effects, Oxidative Stress genetics, Reverse Transcriptase Polymerase Chain Reaction, Staphylococcus aureus metabolism, Staphylococcus aureus pathogenicity, Up-Regulation drug effects, Urease genetics, Urease metabolism, Virulence Factors genetics, Virulence Factors metabolism, Ethanol pharmacology, Gene Expression Regulation, Bacterial drug effects, Staphylococcus aureus drug effects, Staphylococcus aureus genetics
Abstract

It was recently shown that, as in yeast, alcohols selectively increase the hemolytic properties of certain staphylococci strains. This phenomenon has been called 'microbial alcohol-conferred hemolysis'(MACH). Here we present the changes in gene expression by Staphylococcus aureus 8325-4, in response to ethanol. Ethanol upregulated the expression of multiple toxins and increase the pathogen potential of S. aureus strain 8325-4. Ethanol also increased the level of genes considered necessary for production and viability of biofilm, such as: icaAD, sdrDE, pyr, and ure. Increased urease activity appeared to be an important factor in the ethanol response along with macromolecule repair mechanisms. Oxidative-stress responses, such as increased expression of sodA1, sodA2 and upregulation of zinc-containing alcohol dehydrogenase, alcohol-acetaldehyde dehydrogenase (adhE) and two aldehyde dehydrogenases (aldA1, aldA2), which can generate more reducing power, were also induced. Upregulation of fatty acid metabolism appears to be important in enabling the bacteria to handle excess amounts of ethanol which ultimately may lead to synthesis of lytic lypids. The patterns of regulation were confirmed by quantitive reverse transcriptase PCR (QRT-PCR). These results, taken together, suggest that exposure to ethanol increases pathogenic traits and induce oxidative-stress responses.

Published
2010
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3. Alcohol increases hemolysis by staphylococci.

Author

Korem M, Gov Y, Shirron N, Shuster A, and Rosenberg M

Subjects
Bacterial Proteins biosynthesis, Bacterial Proteins genetics, Hemolysin Proteins biosynthesis, Hemolysin Proteins genetics, Hydrogen Peroxide pharmacology, RNA, Messenger metabolism, Staphylococcus aureus pathogenicity, Staphylococcus epidermidis pathogenicity, Up-Regulation, Virulence Factors biosynthesis, Virulence Factors genetics, 1-Butanol pharmacology, Ethanol pharmacology, Hemolysis drug effects, Staphylococcus aureus drug effects, Staphylococcus epidermidis drug effects
Abstract

It was recently found that alcohols can confer hemolytic properties on certain species of yeast. Here, it is reported that alcohol can promote hemolysis by various species of staphylococci, including strains of Staphylococcus aureus, Staphylococcus epidermidis and Staphylococcus hominis. In order to study this novel phenomenon in S. aureus and S. epidermidis, strains that exhibit this phenomenon (e.g. S. aureus 8325-4, COL, SH1000, S. epidermidis), as compared with strains that exhibited little alcohol-enhanced hemolysis (e.g. S. aureus 8325-4 DeltaTRAP, RN6911) were examined. Both ethanol and n-butanol caused upregulation of the virulence regulator-RNAIII, with a concomitant increase in the production of alpha, beta and gamma-hemolysins in strain 8325-4. In S. aureus COL and SH1000, there was an increase in RNAIII but no change in transcription levels of alpha, beta and gamma hemolysins. Staphylococcus epidermidis stain sofi exhibited increased RNAIII and beta hemolysin production. Staphylococcus aureus mutant strains (8325-4 DeltaTRAP and RN6911) showed no change in the transcription level of the RNAIII regulator and the above hemolysins. Increased hemolysis in S. aureus COL, SH1000 and mutant strains may be caused by other hemolysins (not regulated by RNAIII) or through other mechanisms such as hyperoxidation or cytotoxic lipids.

Published
2007
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4. Transcriptional profiling of target of RNAIII-activating protein, a master regulator of staphylococcal virulence.

Author

Korem M, Gov Y, Kiran MD, and Balaban N

Subjects
Adaptor Proteins, Signal Transducing, Bacterial Proteins genetics, Bacterial Proteins physiology, Biofilms growth & development, Gene Expression Profiling, Monomeric GTP-Binding Proteins metabolism, Oligonucleotide Array Sequence Analysis, Phosphoproteins genetics, Phosphoproteins physiology, Phosphorylation, RNA Polymerase III metabolism, Trans-Activators metabolism, Transcription, Genetic, Virulence genetics, Bacterial Proteins metabolism, Gene Expression Regulation, Bacterial, Phosphoproteins metabolism, Staphylococcus aureus genetics, Staphylococcus aureus pathogenicity
Abstract

Staphylococcus aureus is a gram-positive bacterium that is part of the normal healthy flora but that can become virulent and cause infections by producing biofilms and toxins. The production of virulence factors is regulated by cell-cell communication (quorum sensing) through the histidine phosphorylation of target of RNAIII-activating protein (TRAP), which is a 21-kDa protein that is highly conserved among staphylococci. Using microarray analysis, we show here that the expression and phosphorylation of TRAP upregulate the expression of most, if not all, toxins known to date, as well as their global regulator agr. In addition, we show here that the expression and phosphorylation of TRAP are also necessary for the expression of genes known to be necessary for the survival of the bacteria in a biofilm, like arc, pyr, and ure. TRAP is thus demonstrated to be a master regulator of staphylococcal pathogenesis.

Published
2005
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5. Quorum sensing in Staphylococci is regulated via phosphorylation of three conserved histidine residues.

Author

Gov Y, Borovok I, Korem M, Singh VK, Jayaswal RK, Wilkinson BJ, Rich SM, and Balaban N

Subjects
Amino Acid Sequence, Animals, Blotting, Northern, Cell Communication, DNA metabolism, Electrophoresis, Polyacrylamide Gel, Escherichia coli metabolism, Mice, Molecular Sequence Data, Mutagenesis, Mutagenesis, Site-Directed, Mutation, Phenotype, Phosphorylation, Phylogeny, Plasmids metabolism, Protein Structure, Tertiary, RNA, Antisense chemistry, RNA, Bacterial chemistry, Sequence Homology, Amino Acid, Signal Transduction, Time Factors, Histidine chemistry, Staphylococcus aureus metabolism
Abstract

Staphylococcus aureus cause infections by producing toxins, a process regulated by cell-cell communication (quorum sensing) through the histidine-phosphorylation of the target of RNAIII-activating protein (TRAP). We show here that TRAP is highly conserved in staphylococci and contains three completely conserved histidine residues (His-66, His-79, His-154) that are phosphorylated and essential for its activity. This was tested by constructing a TRAP(-) strain with each of the conserved histidine residues changed to alanine by site-directed mutagenesis. All mutants were tested for pathogenesis in vitro (expression of RNAIII and hemolytic activity) and in vivo (murine cellulitis model). Results show that RNAIII is not expressed in the TRAP(-) strain, that it is non hemolytic, and that it does not cause disease in vivo. These pathogenic phenotypes could be rescued in the strain containing the recovered traP, confirming the importance of TRAP in S. aureus pathogenesis. The phosphorylation of TRAP mutated in any of the conserved histidine residues was significantly reduced, and mutants defective in any one of these residues were non-pathogenic in vitro or in vivo, whereas those mutated in a non-conserved histidine residue (His-124) were as pathogenic as the wild type. These results confirm the importance of the three conserved histidine residues in TRAP activity. The phosphorylation pattern, structure, and gene organization of TRAP deviates from signaling molecules known to date, suggesting that TRAP belongs to a novel class of signal transducers.

Published
2004
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6. Characterization of RAP, a quorum sensing activator of Staphylococcus aureus.

Author

Korem M, Sheoran AS, Gov Y, Tzipori S, Borovok I, and Balaban N

Subjects
Adaptor Proteins, Signal Transducing, Amino Acid Sequence, Animals, Antibodies, Monoclonal, Carrier Proteins immunology, Carrier Proteins metabolism, Female, Gene Expression Regulation, Bacterial, Mice, Mice, Inbred BALB C, Molecular Sequence Data, Phosphoproteins metabolism, RNA, Antisense metabolism, RNA, Bacterial metabolism, Recombinant Proteins genetics, Recombinant Proteins immunology, Recombinant Proteins metabolism, Staphylococcus aureus metabolism, Staphylococcus aureus pathogenicity, Virulence, Bacterial Proteins, Carrier Proteins genetics, Staphylococcal Infections microbiology, Staphylococcus aureus genetics
Abstract

Staphylococcus aureus are Gram-positive bacteria and cause diverse serious diseases in humans and animals through the production of toxins. The production of toxins is regulated by quorum sensing mechanisms, where proteins such as RNAIII activating protein (RAP) are secreted by the bacteria and induce virulence. Antibodies to RAP have been shown to protect mice from infection, but the molecular structure of RAP was not known and hindered vaccine development. To characterize RAP, recombinant protein was made and tested for its ability to induce genes important for pathogenesis (agr). In addition, monoclonal antibodies were produced to identify its cellular localization. Results shown here indicate that RAP is a 277-aa protein that is an ortholog of the ribosomal protein L2. Like the native molecule, recombinant RAP activates the production of RNAIII (encoded by agr). Using RAP specific monoclonal antibodies we demonstrate that RAP is continuously secreted and while RAP is expressed also in other bacteria (like Staphylococcus epidermidis, Staphylococcus xylosus and Escherichia coli), it is secreted to the culture medium only by S. aureus. Our results show that the ribosomal protein L2 has an extraribosomal function and that when secreted RAP acts as an autoinducer of virulence to regulate S. aureus pathogenesis.

Published
2003
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7. Infective Endocarditis in Patients on Chronic Hemodialysis

Author

Juan M. Pericàs, Jaume Llopis, Maria Jesús Jiménez-Exposito, Wissam M. Kourany, Benito Almirante, Giampiero Carosi, Emanuele Durante-Mangoni, Claudio Querido Fortes, Efthymia Giannitsioti, Stamatios Lerakis, Rodrigo Montagna-Mella, Juan Ambrosioni, Ru-San Tan, Carlos A. Mestres, Dannah Wray, Orathai Pachirat, Asuncion Moreno, Vivian H. Chu, Elisa de Lazzari, Vance G. Fowler, Jose M. Miró, Liliana Clara, Marisa Sanchez, José Casabé, Claudia Cortes, Francisco Nacinovich, Pablo Fernandez Oses, Ricardo Ronderos, Adriana Sucari, Jorge Thierer, Javier Altclas, Silvia Kogan, Denis Spelman, Eugene Athan, Owen Harris, Karina Kennedy, Ren Tan, David Gordon, Lito Papanicolas, Tony Korman, Despina Kotsanas, Robyn Dever, Phillip Jones, Pam Konecny, Richard Lawrence, David Rees, Suzanne Ryan, Michael P. Feneley, John Harkness, Jeffrey Post, Porl Reinbott, Rainer Gattringer, Franz Wiesbauer, Adriana Ribas Andrade, Ana Cláudia Passos de Brito, Armenio Costa Guimarães, Max Grinberg, Alfredo José Mansur, Rinaldo Focaccia Siciliano, Tania Mara Varejao Strabelli, Marcelo Luiz Campos Vieira, Regina Aparecida de Medeiros Tranchesi, Marcelo Goulart Paiva, Auristela de Oliveira Ramos, Clara Weksler, Giovanna Ferraiuoli, Wilma Golebiovski, Cristiane Lamas, James A. Karlowsky, Yoav Keynan, Andrew M. Morris, Ethan Rubinstein, Sandra Braun Jones, Patricia Garcia, M. Cereceda, Alberto Fica, Rodrigo Montagna Mella, Ricardo Fernandez, Liliana Franco, Javier Gonzalez, Astrid Natalia Jaramillo, Bruno Barsic, Suzana Bukovski, Vladimir Krajinovic, Ana Pangercic, Igor Rudez, Josip Vincelj, Tomas Freiberger, Jiri Pol, Barbora Zaloudikova, Zainab Ashour, Amani El Kholy, Marwa Mishaal, Dina Osama, Hussien Rizk, Neijla Aissa, Corentine Alauzet, Francois Alla, CHU Catherine Campagnac, Thanh Doco-Lecompte, Christine Selton-Suty, Jean-Paul Casalta, Pierre-Edouard Fournier, Gilbert Habib, Didier Raoult, Franck Thuny, Francois Delahaye, Armelle Delahaye, Francois Vandenesch, Erwan Donal, Pierre Yves Donnio, Erwan Flecher, Christian Michelet, Matthieu Revest, Pierre Tattevin, Florent Chevalier, Antoine Jeu, Jean Paul Rémadi, Dan Rusinaru, Christophe Tribouilloy, Yvette Bernard, Catherine Chirouze, Bruno Hoen, Joel Leroy, Patrick Plesiat, Christoph Naber, Carl Neuerburg, Bahram Mazaheri, Carl Neuerburg Sophia Athanasia, Ioannis Deliolanis, Helen Giamarellou, Tsaganos Thomas, Elena Mylona, Olga Paniara, Konstantinos Papanicolaou, John Pyros, Athanasios Skoutelis, Konstantinos Papanikolaou, Gautam Sharma, Johnson Francis, Lathi Nair, Vinod Thomas, Krishnan Venugopal, Margaret M. Hannan, John P. Hurley, Maor Wanounou, Dan Gilon, Sarah Israel, Maya Korem, Jacob Strahilevitz, Domenico Iossa, Serena Orlando, Maria Paola Ursi, Pia Clara Pafundi, Fabiana D’Amico, Mariano Bernardo, Susanna Cuccurullo, Giovanni Dialetto, Franco Enrico Covino, Sabrina Manduca, Alessandro Della Corte, Marisa De Feo, Marie Françoise Tripodi, Enrico Cecchi, Francesco De Rosa, Davide Forno, Massimo Imazio, Rita Trinchero, Paolo Grossi, Mariangela Lattanzio, Antonio Toniolo, Antonio Goglio, Annibale Raglio, Veronica Ravasio, Marco Rizzi, Fredy Suter, Silvia Magri, Liana Signorini, Zeina Kanafani, Souha S. Kanj, Ahmad Sharif-Yakan, Imran Abidin, Syahidah Syed Tamin, Eduardo Rivera Martínez, Gabriel Israel Soto Nieto, Jan T.M. van der Meer, Stephen Chambers, David Holland, Arthur Morris, Nigel Raymond, Kerry Read, David R. Murdoch, Stefan Dragulescu, Adina Ionac, Cristian Mornos, O.M. Butkevich, Natalia Chipigina, Ozerecky Kirill, Kulichenko Vadim, Tatiana Vinogradova, Jameela Edathodu, Magid Halim, Yee-Yun Liew, Tatjana Lejko-Zupanc, Mateja Logar, Manica Mueller-Premru, Patrick Commerford, Anita Commerford, Eduan Deetlefs, Cass Hansa, Mpiko Ntsekhe, Manel Almela, Manuel Azqueta, Merce Brunet, Pedro Castro, Elisa De Lazzari, Carlos Falces, David Fuster, Guillermina Fita, Cristina Garcia- de- la- Maria, Javier Garcia-Gonzalez, Jose M. Gatell, Francesc Marco, José M. Miró, José Ortiz, Salvador Ninot, J. Carlos Paré, Juan M. Pericas, Eduard Quintana, Jose Ramirez, Irene Rovira, Elena Sandoval, Marta Sitges, Adrian Tellez, José M. Tolosana, Barbara Vidal, Jordi Vila, Ignasi Anguera, Bernat Font, Joan Raimon Guma, Javier Bermejo, Emilio Bouza, Miguel Angel Garcia Fernández, Victor Gonzalez-Ramallo, Mercedes Marín, Patricia Muñoz, Miguel Pedromingo, Jorge Roda, Marta Rodríguez-Créixems, Jorge Solis, Nuria Fernandez-Hidalgo, Pilar Tornos, Arístides de Alarcón, Ricardo Parra, Eric Alestig, Magnus Johansson, Lars Olaison, Ulrika Snygg-Martin, Pimchitra Pachirat, Burabha Pussadhamma, Vichai Senthong, Anna Casey, Tom Elliott, Peter Lambert, Richard Watkin, Christina Eyton, John L. Klein, Suzanne Bradley, Carol Kauffman, Roger Bedimo, G. Ralph Corey, Anna Lisa Crowley, Pamela Douglas, Laura Drew, Thomas Holland, Tahaniyat Lalani, Daniel Mudrick, Zaniab Samad, Daniel Sexton, Martin Stryjewski, Andrew Wang, Christopher W. Woods, Robert Cantey, Lisa Steed, Stuart A. Dickerman, Hector Bonilla, Joseph DiPersio, Sara-Jane Salstrom, John Baddley, Mukesh Patel, Gail Peterson, Amy Stancoven, Donald Levine, Jonathan Riddle, Michael Rybak, Christopher H. Cabell, Pericas, J. M., Llopis, J., Jimenez-Exposito, M. J., Kourany, W. M., Almirante, B., Carosi, G., Durante-Mangoni, E., Fortes, C. Q., Giannitsioti, E., Lerakis, S., Montagna-Mella, R., Ambrosioni, J., Tan, R. -S., Mestres, C. A., Wray, D., Pachirat, O., Moreno, A., Chu, V. H., de Lazzari, E., Fowler, V. G., Miro, J. M., Clara, L., Sanchez, M., Casabe, J., Cortes, C., Nacinovich, F., Oses, P. F., Ronderos, R., Sucari, A., Thierer, J., Altclas, J., Kogan, S., Spelman, D., Athan, E., Harris, O., Kennedy, K., Tan, R., Gordon, D., Papanicolas, L., Korman, T., Kotsanas, D., Dever, R., Jones, P., Konecny, P., Lawrence, R., Rees, D., Ryan, S., Feneley, M. P., Harkness, J., Post, J., Reinbott, P., Gattringer, R., Wiesbauer, F., Andrade, A. R., Passos de Brito, A. C., Guimaraes, A. C., Grinberg, M., Mansur, A. J., Siciliano, R. F., Varejao Strabelli, T. M., Campos Vieira, M. L., de Medeiros Tranchesi, R. A., Paiva, M. G., de Oliveira Ramos, A., Weksler, C., Ferraiuoli, G., Golebiovski, W., Lamas, C., Karlowsky, J. A., Keynan, Y., Morris, A. M., Rubinstein, E., Jones, S. B., Garcia, P., Cereceda, M., Fica, A., Mella, R. M., Fernandez, R., Franco, L., Gonzalez, J., Jaramillo, A. N., Barsic, B., Bukovski, S., Krajinovic, V., Pangercic, A., Rudez, I., Vincelj, J., Freiberger, T., Pol, J., Zaloudikova, B., Ashour, Z., El Kholy, A., Mishaal, M., Osama, D., Rizk, H., Aissa, N., Alauzet, C., Alla, F., Campagnac, C. C., Doco-Lecompte, T., Selton-Suty, C., Casalta, J. -P., Fournier, P. -E., Habib, G., Raoult, D., Thuny, F., Delahaye, F., Delahaye, A., Vandenesch, F., Donal, E., Donnio, P. Y., Flecher, E., Michelet, C., Revest, M., Tattevin, P., Chevalier, F., Jeu, A., Remadi, J. P., Rusinaru, D., Tribouilloy, C., Bernard, Y., Chirouze, C., Hoen, B., Leroy, J., Plesiat, P., Naber, C., Neuerburg, C., Mazaheri, B., Sophia Athanasia, C. N., Deliolanis, I., Giamarellou, H., Thomas, T., Mylona, E., Paniara, O., Papanicolaou, K., Pyros, J., Skoutelis, A., Papanikolaou, K., Sharma, G., Francis, J., Nair, L., Thomas, V., Venugopal, K., Hannan, M. M., Hurley, J. P., Wanounou, M., Gilon, D., Israel, S., Korem, M., Strahilevitz, J., Iossa, D., Orlando, S., Ursi, M. P., Pafundi, P. C., D'Amico, F., Bernardo, M., Cuccurullo, S., Dialetto, G., Covino, F. E., Manduca, S., Della Corte, A., De Feo, M., Tripodi, M. F., Cecchi, E., De Rosa, F., Forno, D., Imazio, M., Trinchero, R., Grossi, P., Lattanzio, M., Toniolo, A., Goglio, A., Raglio, A., Ravasio, V., Rizzi, M., Suter, F., Magri, S., Signorini, L., Kanafani, Z., Kanj, S. S., Sharif-Yakan, A., Abidin, I., Tamin, S. S., Martinez, E. R., Soto Nieto, G. I., van der Meer, J. T. M., Chambers, S., Holland, D., Morris, A., Raymond, N., Read, K., Murdoch, D. R., Dragulescu, S., Ionac, A., Mornos, C., Butkevich, O. M., Chipigina, N., Kirill, O., Vadim, K., Vinogradova, T., Edathodu, J., Halim, M., Liew, Y. -Y., Lejko-Zupanc, T., Logar, M., Mueller-Premru, M., Commerford, P., Commerford, A., Deetlefs, E., Hansa, C., Ntsekhe, M., Almela, M., Azqueta, M., Brunet, M., Castro, P., Falces, C., Fuster, D., Fita, G., Garcia- de- la- Maria, C., Garcia-Gonzalez, J., Gatell, J. M., Marco, F., Ortiz, J., Ninot, S., Pare, J. C., Quintana, E., Ramirez, J., Rovira, I., Sandoval, E., Sitges, M., Tellez, A., Tolosana, J. M., Vidal, B., Vila, J., Anguera, I., Font, B., Guma, J. R., Bermejo, J., Bouza, E., Garcia Fernandez, M. A., Gonzalez-Ramallo, V., Marin, M., Munoz, P., Pedromingo, M., Roda, J., Rodriguez-Creixems, M., Solis, J., Fernandez-Hidalgo, N., Tornos, P., de Alarcon, A., Parra, R., Alestig, E., Johansson, M., Olaison, L., Snygg-Martin, U., Pachirat, P., Pussadhamma, B., Senthong, V., Casey, A., Elliott, T., Lambert, P., Watkin, R., Eyton, C., Klein, J. L., Bradley, S., Kauffman, C., Bedimo, R., Corey, G. R., Crowley, A. L., Douglas, P., Drew, L., Holland, T., Lalani, T., Mudrick, D., Samad, Z., Sexton, D., Stryjewski, M., Wang, A., Woods, C. W., Cantey, R., Steed, L., Dickerman, S. A., Bonilla, H., Dipersio, J., Salstrom, S. -J., Baddley, J., Patel, M., Peterson, G., Stancoven, A., Levine, D., Riddle, J., Rybak, M., Cabell, C. H., Bristol-Myers Squibb Company, Vall d'Hebron University Hospital [Barcelona], Laboratoire Chrono-environnement - CNRS - UBFC (UMR 6249) (LCE), Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon), Centre recherche en CardioVasculaire et Nutrition = Center for CardioVascular and Nutrition research (C2VN), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), CHU Pontchaillou [Rennes], ARN régulateurs bactériens et médecine (BRM), 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 ), and Laboratoire Chrono-environnement (UMR 6249) (LCE)

Subjects
Male, relapses, medicine.medical_treatment, infective endocarditi, 030204 cardiovascular system & hematology, Kidney Failure, Cohort Studies, Catheters, Indwelling, 0302 clinical medicine, Surgical, Epidemiology, cardiac surgery, enterococci, hemodialysis, infective endocarditis, Staphylococcus aureus, Aged, Anti-Bacterial Agents, Arteriovenous Shunt, Surgical, Cardiac Surgical Procedures, Endocarditis, Female, Humans, Kidney Failure, Chronic, Methicillin-Resistant Staphylococcus aureus, Middle Aged, Renal Dialysis, Staphylococcal Infections, 030212 general & internal medicine, Chronic, Prospective cohort study, health care economics and organizations, relapse, Arteriovenous Shunt, 3. Good health, Cardiac surgery, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Indwelling, Infective endocarditis, Hemodialysis, Cardiology and Cardiovascular Medicine, medicine.medical_specialty, Catheters, education, 03 medical and health sciences, Internal medicine, medicine, business.industry, medicine.disease, hemodialysi, Etiology, Complication, business, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; Background - Infective endocarditis (IE) is a common and serious complication in patients receiving chronic hemodialysis (HD). Objectives - This study sought to investigate whether there are significant differences in complications, cardiac surgery, relapses, and mortality between IE cases in HD and non-HD patients. Methods - Prospective cohort study (International Collaboration on Endocarditis databases, encompassing 7,715 IE episodes from 2000 to 2006 and from 2008 to 2012). Descriptive analysis of baseline characteristics, epidemiological and etiological features, complications and outcomes, and their comparison between HD and non-HD patients was performed. Risk factors for major embolic events, cardiac surgery, relapses, and in-hospital and 6-month mortality were investigated in HD-patients using multivariable logistic regression. Results - A total of 6,691 patients were included and 553 (8.3%) received HD. North America had a higher HD-IE proportion than the other regions. The predominant microorganism was Staphylococcus aureus (47.8%), followed by enterococci (15.4%). Both in-hospital and 6-month mortality were significantly higher in HD versus non-HD-IE patients (30.4% vs. 17% and 39.8% vs. 20.7%, respectively; p

Published
2021
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