31 results on '"Fernandez-Barat L"'
Search Results
2. Clustering ARDS Patients Through the First Days of ICU Admission
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Ceccato, A., primary, Forne, C., additional, Bos, L.D.J., additional, Camprubí-Rimblas, M., additional, Areny-Balagueró, A., additional, Campaña Duel, E., additional, Quero, S., additional, Diaz, E., additional, Roca, O., additional, De Gonzalo-Calvo, D., additional, Fernandez-Barat, L., additional, Motos, A., additional, Ferrer, R., additional, Lorente, J., additional, Menendez, R., additional, Barbe, F., additional, Calfee, C.S., additional, Torres, A., additional, and Artigas, A., additional
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- 2024
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3. Pseudomonas Aeruginosa and Bronchiectasis: Pathogenicity and Immune Response in Patients Exacerbated and Not Exacerbated
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Cabrera, R., primary, Vázquez, N., additional, Lopez-Aladid, R., additional, Bueno, L., additional, Amaro, R., additional, Muñoz, L., additional, Vila, J., additional, Fernandez-Barat, L., additional, and Torres, A., additional
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- 2023
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4. Effects of intubation timing in patients with COVID-19 throughout the four waves of the pandemic: a matched analysis
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Universitat Rovira i Virgili, Riera, J; Barbeta, E; Tormos, A; Mellado-Artigas, R; Ceccato, A; Motos, A; Fernandez-Barat, L; Ferrer, R; Garcia-Gasulla, D; Penuelas, O; Lorente, JA; Menendez, R; Roca, O; Palomeque, A; Ferrando, C; Sole-Violan, J; Novo, M; Boado, MV; Tamayo, L; Estella, A; Galban, C; Trenado, J; Huerta, A; Loza, A; Aguilera, L; Garmendia, JLG; Barbera, C; Gumucio, V; Socias, L; Franco, N; Valdivia, LJ; Vidal, P; Sagredo, V; Ruiz-Garcia, AL; Varela, IM; Lopez, J; Pozo, JC; Nieto, M; Gomez, JM; Blandino, A; Valledor, M; Bustamante-Munguira, E; Sanchez-Miralles, A; Penasco, Y; Barberan, J; Ubeda, A; Amaya-Villar, R; Martin, MC; Jorge, R; Caballero, J; Marin, J; Anon, JM; Sipmann, FS; Albaiceta, GM; Castellanos-Ortega, A; Adell-Serrano, B; Catalan, M; Gandara, AMD; Ricart, P; Carbajales, C; Rodriguez, A; Diaz, E; Torre, MCD; Gallego, E; Canton-Bulnes, L; Carbonell, N; Gonzalez, J; de Gonzalo-Calvo, D; Barbe, F; Torres, A, Universitat Rovira i Virgili, and Riera, J; Barbeta, E; Tormos, A; Mellado-Artigas, R; Ceccato, A; Motos, A; Fernandez-Barat, L; Ferrer, R; Garcia-Gasulla, D; Penuelas, O; Lorente, JA; Menendez, R; Roca, O; Palomeque, A; Ferrando, C; Sole-Violan, J; Novo, M; Boado, MV; Tamayo, L; Estella, A; Galban, C; Trenado, J; Huerta, A; Loza, A; Aguilera, L; Garmendia, JLG; Barbera, C; Gumucio, V; Socias, L; Franco, N; Valdivia, LJ; Vidal, P; Sagredo, V; Ruiz-Garcia, AL; Varela, IM; Lopez, J; Pozo, JC; Nieto, M; Gomez, JM; Blandino, A; Valledor, M; Bustamante-Munguira, E; Sanchez-Miralles, A; Penasco, Y; Barberan, J; Ubeda, A; Amaya-Villar, R; Martin, MC; Jorge, R; Caballero, J; Marin, J; Anon, JM; Sipmann, FS; Albaiceta, GM; Castellanos-Ortega, A; Adell-Serrano, B; Catalan, M; Gandara, AMD; Ricart, P; Carbajales, C; Rodriguez, A; Diaz, E; Torre, MCD; Gallego, E; Canton-Bulnes, L; Carbonell, N; Gonzalez, J; de Gonzalo-Calvo, D; Barbe, F; Torres, A
- Abstract
Background The primary aim of our study was to investigate the association between intubation timing and hospital mortality in critically ill patients with coronavirus disease 2019 (COVID-19)-associated respiratory failure. We also analysed both the impact of such timing throughout the first four pandemic waves and the influence of prior noninvasive respiratory support on outcomes.Methods This is a secondary analysis of a multicentre, observational and prospective cohort study that included all consecutive patients undergoing invasive mechanical ventilation due to COVID-19 from across 58 Spanish intensive care units (ICUs) participating in the CIBERESUCICOVID project. The study period was between 29 February 2020 and 31 August 2021. Early intubation was defined as that occurring within the first 24 h of ICU admission. Propensity score matching was used to achieve a balance across baseline variables between the early intubation cohort and those patients who were intubated after the first 24 h of ICU admission. Differences in outcomes between early and delayed intubation were also assessed. We performed sensitivity analyses to consider a different time-point (48 h from ICU admission) for early and delayed intubation.Results Of the 2725 patients who received invasive mechanical ventilation, a total of 614 matched patients were included in the analysis (307 for each group). In the unmatched population, there were no differences in mortality between the early and delayed groups. After propensity score matching, patients with delayed intubation presented higher hospital mortality (27.3% versus 37.1%; p=0.01), ICU mortality (25.7% versus 36.1%; p=0.007) and 90-day mortality (30.9% versus 40.2%; p=0.02) compared with the early intubation group. Very similar findings were observ
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- 2023
5. Identification of highly immunogenic epitopes in the SARS-CoV-2 Spike protein to produce monoclonal antibodies
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Fernandez Barat, L, primary, López-Aladid, R, additional, Bueno, L, additional, Farriol, R, additional, Porta, E, additional, López-Gavin, À, additional, Motos, A, additional, Aguilar, R, additional, Vidal, M, additional, Jiménez, A, additional, Cabrera, R, additional, Vázquez, N, additional, Barbeta, E, additional, Ferrer, M, additional, Palomeque, A C, additional, Moncunill, G, additional, Lozano, M, additional, Garcia-Basteiro, A, additional, Dobaño, C, additional, and Torres, A, additional
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- 2022
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6. Risk factors for mortality in COPD patients with COVID-19 admitted to Intensive Care Unit
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Fernandez Barat, L, primary, Alvarez-Napagao, S, additional, Barroso, M, additional, Motos, A, additional, Gabarrús, A, additional, Ceccato, A, additional, Pérez, R, additional, García, D, additional, Battaglini, D, additional, Palomeque, A, additional, Bermejo, J, additional, Barbé, F, additional, and Torres, A, additional
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- 2022
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7. Relationship between the microbiome and the GOLD Stage during exacerbations
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Lopez-Aladid, R, primary, Fernandez Barat, L, additional, Bueno-Freire, L, additional, Ceccato, A, additional, Huerta, A, additional, Soler, N, additional, and Torres, A, additional
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- 2022
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8. The Mucoid Pathobiome and Its Clinical Implications in Non-Cystic Fibrosis Bronchiectasis
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Fernandez-Barat, L., primary, López-Aladid, R., additional, Alcaraz, V., additional, Vázquez, N., additional, Bueno, L., additional, Pastor, R., additional, Lingren, L., additional, Sanz, H., additional, Oscanoa, P., additional, Amaro, R., additional, Motos, A., additional, Cabrera, R., additional, Vila, J., additional, Martínez, D., additional, Otero, J., additional, Farre, R., additional, Hoiby, N., additional, and Torres, A., additional
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- 2022
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9. Identification of Highly Immunogenic Epitopes in the SARS-CoV-2 Spike Protein to Produce Neutralizing Monoclonal Antibodies for Treatment
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Lopez-Aladid, R., primary, Bueno-Freire, L., additional, Farriol, R., additional, Porta, E., additional, López-Gavin, A., additional, Motos, A., additional, Aguilar, R., additional, Vidal, M., additional, Jimenez, A., additional, Cabrera, R., additional, Vazquez, N., additional, Barbeta, E., additional, Ferrer, M., additional, Palomeque, A.C., additional, Moncunill, G., additional, Lozano, M., additional, Garcia-Basteiro, A., additional, Dobaño, C., additional, Fernandez-Barat, L., additional, and Torres, A., additional
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- 2022
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10. Tracheal tube biofilm removal through a novel closed-suctioning system: an experimental study
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Aguilera Xiol, E., Li Bassi, G., Wyncoll, D., Ntoumenopoulos, G., Fernandez-Barat, L., Marti, J. D., Comaru, T., De Rosa, F., Rigol, M., Rinaudo, M., Ferrer, M., and Torres, A.
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- 2015
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11. The evolution of the ventilatory ratio is a prognostic factor in mechanically ventilated COVID-19 ARDS patients (vol 25, 331, 2021)
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Torres, A, Motos, A, Riera, J, Fernandez-Barat, L, Ceccato, A, Perez-Arnal, R, Garcia-Gasulla, D, Penuelas, O, Lorente, JA, Rodriguez, A, de Gonzalo-Calvo, D, Almansa, R, Gabarrus, A, Menendez, R, Bermejo-Martin, JF, Ferrer, R, Villar, RA, Anon, JM, Barbera, C, Barberan, J, Ortiz, AB, Bustamante-Munguira, E, Caballero, J, Carbajales, C, Carbonell, N, Catalan-Gonzalez, M, Galban, C, Gumucio-Sanguino, VD, de la Torre, MD, Diaz, E, Estella, A, Gallego, E, Garmendia, JLG, Garnacho-Montero, J, Gomez, JM, Huerta, A, Garcia, RNJ, Loza-Vazquez, A, Marin-Corral, J, de la Gandara, AM, Varela, IM, Messa, JL, Albaiceta, GM, Novo, MA, Penasco, Y, Pozo-Laderas, JC, Ricart, P, Salvador-Adell, I, Sanchez-Miralles, A, Chinesta, SS, Socias, L, Sole-Violan, J, Sipmann, FS, Lomas, LT, Trenado, J, and Barbe, F
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- 2021
12. Development and characterization of a novel model of invasive pneumococcal pneumonia in invasively ventilated PIGS
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Li Bassi, G, Amaro, R, Chiurazzi, C, Aguilera Xiol, E, Travierso, C, Fernandez Barat, L, Motos, A, Schultz, M, Carbonara, M, Rigol, M, Marti, D, Saco, M, Comaru, T, Ramirez, J, and Torres, A
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- 2015
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13. Efficacy of Telavancin in Comparison to Linezolid in a Porcine Model of Severe Methicillin-Resistant Staphylococcus aureus Pneumonia
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Battaglini, D., primary, Motos, A., additional, Li Bassi, G., additional, Yang, H., additional, Pagliara, F., additional, Yang, M., additional, Aguilera Xiol, E., additional, Meli, A., additional, Bobi, J., additional, Frigola, G., additional, Senussi, T., additional, Idone, F., additional, Travierso, C., additional, Chiurazzi, C., additional, Fernandez-Barat, L., additional, Rigol, M., additional, Ramirez, J., additional, Pelosi, P., additional, Chiumello, D., additional, Antonelli, M., additional, Nicolau, D. P., additional, Bringue, J., additional, Artigas, A., additional, Guerrero, L., additional, Soy, D., additional, and Torres, A., additional
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- 2020
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14. Factors Associated With One-Year Mortality in Hospitalised Patients With Exacerbated Bronchiectasis
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Scioscia, G., Alcaraz-Serrano, V., Méndez, R., Gabarrús, A., Fernández-Barat, L., Menéndez, R., Tondo, P., Bueno, L., and Torres, A.
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- 2022
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15. Nebulized Amikacin and Fosfomycin for Severe Pseudomonas aeruginosa Pneumonia: An Experimental Study
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Li Bassi, G., Motos, A., Fernandez-Barat, L., Aguilera Xiol, E., Chiurazzi, C., Senussi, T., Saco, M. A., Fuster, C., Carbonara, M., Bobi, J., Amaro, R., De Rosa, F., Comaru, T., Yang, H., Ranzani, O. T., Marti, J. -D., Rinaudo, M., Comino Trinidad, O., Rigol, M., Bringue, J., Ramirez, J., Nicolau, D. P., Pelosi, P., Antonelli, Massimo, Blasi, F., Artigas, A., Montgomery, A. B., Torres, A., Antonelli M. (ORCID:0000-0003-3007-1670), Li Bassi, G., Motos, A., Fernandez-Barat, L., Aguilera Xiol, E., Chiurazzi, C., Senussi, T., Saco, M. A., Fuster, C., Carbonara, M., Bobi, J., Amaro, R., De Rosa, F., Comaru, T., Yang, H., Ranzani, O. T., Marti, J. -D., Rinaudo, M., Comino Trinidad, O., Rigol, M., Bringue, J., Ramirez, J., Nicolau, D. P., Pelosi, P., Antonelli, Massimo, Blasi, F., Artigas, A., Montgomery, A. B., Torres, A., and Antonelli M. (ORCID:0000-0003-3007-1670)
- Abstract
OBJECTIVES: Latest trials failed to confirm merits of nebulized amikacin for critically ill patients with nosocomial pneumonia. We studied various nebulized and IV antibiotic regimens in a porcine model of severe Pseudomonas aeruginosa pneumonia, resistant to amikacin, fosfomycin, and susceptible to meropenem. DESIGN: Prospective randomized animal study. SETTING: Animal Research, University of Barcelona, Spain. SUBJECTS: Thirty female pigs. INTERVENTIONS: The animals were randomized to receive nebulized saline solution (CONTROL); nebulized amikacin every 6 hours; nebulized fosfomycin every 6 hours; IV meropenem alone every 8 hours; nebulized amikacin and fosfomycin every 6 hours; amikacin and fosfomycin every 6 hours, with IV meropenem every 8 hours. Nebulization was performed through a vibrating mesh nebulizer. The primary outcome was lung tissue bacterial concentration. Secondary outcomes were tracheal secretions P. aeruginosa concentration, clinical variables, lung histology, and development of meropenem resistance. MEASUREMENTS AND MAIN RESULTS: We included five animals into each group. Lung P. aeruginosa burden varied among groups (p < 0.001). In particular, IV meropenem and amikacin and fosfomycin + IV meropenem groups presented lower P. aeruginosa concentrations versus amikacin and fosfomycin, amikacin, CONTROL, and fosfomycin groups (p < 0.05), without significant difference between these two groups undergoing IV meropenem treatment. The sole use of nebulized antibiotics resulted in dense P. aeruginosa accumulation at the edges of the interlobular septa. Amikacin, amikacin and fosfomycin, and amikacin and fosfomycin + IV meropenem effectively reduced P. aeruginosa in tracheal secretions (p < 0.001). Pathognomonic clinical variables of respiratory infection did not differ among groups. Resistance to meropenem increased in IV meropenem group versus amikacin and fosfomycin + meropenem (p = 0.004). CONCLUSIONS: Our findings corroborate that amikacin and
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- 2019
16. ESICM LIVES 2016: part three: Milan, Italy. 1–5 October 2016
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Velasquez, T., Mackey, G., Lusk, J., Kyle, U. G., Fontenot, T., Marshall, P., Shekerdemian, L. S., Coss-Bu, J. A., Nishigaki, A., Yatabe, T., Tamura, T., Yamashita, K., Yokoyama, M., Ruiz-Rodriguez, J. C., Encina, B., Belmonte, R., Troncoso, I., Tormos, P., Riveiro, M., Baena, J., Sanchez, A., Bañeras, J., Cordón, J., Duran, N., Ruiz, A., Caballero, J., Nuvials, X., Riera, J., Serra, J., Rutten, A. M. F., van Ieperen, S. N. M., Der Kinderen, E. P. H. M., Van Logten, T., Kovacikova, L., Skrak, P., Zahorec, M., Akcan-Arikan, A., Silva, J. C., Goldsworthy, M., Wood, D., Harrison, D., Parslow, R., Davis, P., Pappachan, J., Goodwin, S., Ramnarayan, P., Chernyshuk, S., Yemets, H., Zhovnir, V., Pulitano’, S. M., De Rosa, S., Mancino, A., Villa, G., Tosi, F., Franchi, P., Conti, G., Patel, B., Khine, H., Shah, A., Sung, D., Singer, L., Haghbin, S., Inaloo, S., Serati, Z., Idei, M., Nomura, T., Yamamoto, N., Sakai, Y., Yoshida, T., Matsuda, Y., Yamaguchi, Y., Takaki, S., Yamaguchi, O., Goto, T., Longani, N., Medar, S., Abdel-Aal, I. R., El Adawy, A. S., Mohammed, H. M. E. H., Mohamed, A. N., Parry, S. M., Knight, L. D., Denehy, L., De Morton, N., Baldwin, C. E., Sani, D., Kayambu, G., da Silva, V. Z. M., Phongpagdi, P., Puthucheary, Z. A., Granger, C. L., Rydingsward, J. E., Horkan, C. M., Christopher, K. B., McWilliams, D., Jones, C., Reeves, E., Atkins, G., Snelson, C., Aitken, L. M., Rattray, J., Kenardy, J., Hull, A. M., Ullman, A., Le Brocque, R., Mitchell, M., Davis, C., Macfarlane, B., Azevedo, J. C., Rocha, L. L., De Freitas, F. F. M., Cavalheiro, A. M., Lucinio, N. M., Lobato, M. S., Ebeling, G., Kraegpoeth, A., Laerkner, E., De Brito-Ashurst, I., White, C., Gregory, S., Forni, L. G., Flowers, E., Curtis, A., Wood, C. A., Siu, K., Venkatesan, K., Muhammad, J. B. H., Ng, L., Seet, E., Baptista, N., Escoval, A., Tomas, E., Agrawal, R., Mathew, R., Varma, A., Dima, E., Charitidou, E., Perivolioti, E., Pratikaki, M., Vrettou, C., Giannopoulos, A., Zakynthinos, S., Routsi, C., Atchade, E., Houzé, S., Jean-Baptiste, S., Thabut, G., Genève, C., Tanaka, S., Lortat-Jacob, B., Augustin, P., Desmard, M., Montravers, P., de Molina, F. J. González, Barbadillo, S., Alejandro, R., Álvarez-Lerma, F., Vallés, J., Catalán, R. M., Palencia, E., Jareño, A., Granada, R. M., Ignacio, M. L., Cui, N., Liu, D., Wang, H., Su, L., Qiu, H., Li, R., Jaffal, K., Rouzé, A., Poissy, J., Sendid, B., Nseir, S., Paramythiotou, E., Rizos, M., Frantzeskaki, F., Antoniadou, A., Vourli, S., Zerva, L., Armaganidis, A., Gottlieb, J., Greer, M., Wiesner, O., Martínez, M., Acuña, M., Rello, J., Welte, T., Mignot, T., Soussi, S., Dudoignon, E., Ferry, A., Chaussard, M., Benyamina, M., Alanio, A., Touratier, S., Chaouat, M., Lafaurie, M., Mimoun, M., Mebazaa, A., Legrand, M., Sheils, M. A., Patel, C., Mohankumar, L., Akhtar, N., Noriega, S. K. Pacheco, Aldana, N. Navarrete, León, J. L. Ávila, Baquero, J. Durand, Bernal, F. Fernández, Ahmadnia, E., Hadley, J. S., Millar, M., Hall, D., Hewitt, H., Yasuda, H., Sanui, M., Komuro, T., Kawano, S., Andoh, K., Yamamoto, H., Noda, E., Hatakeyama, J., Saitou, N., Okamoto, H., Kobayashi, A., Takei, T., Matsukubo, S., Rotzel, H. B., Lázaro, A. Serrano, Prada, D. Aguillón, Gimillo, M. Rodriguez, Barinas, O. Diaz, Cortes, M. L. Blasco, Franco, J. Ferreres, Roca, J. M. Segura, Carratalá, A., Gonçalves, B., Turon, R., Mendes, A., Miranda, F., Mata, P. J., Cavalcanti, D., Melo, N., Lacerda, P., Kurtz, P., Righy, C., Rosario, L. E. de la Cruz, Lesmes, S. P. Gómez, Romero, J. C. García, Herrera, A. N. García, Pertuz, E. D. Díaz, Sánchez, M. J. Gómez, Sanz, E. Regidor, Hualde, J. Barado, Hernández, A. Ansotegui, Irazabal, J. M. Guergué, Spatenkova, V., Bradac, O., Suchomel, P., Urli, T., Lazzeri, E. Heusch, Aspide, R., Zanello, M., Perez-Borrero, L., Garcia-Alvarez, J. M., Arias-Verdu, M. D., Aguilar-Alonso, E., Rivera-Fernandez, R., Mora-Ordoñez, J., De La Fuente-Martos, C., Castillo-Lorente, E., Guerrero-Lopez, F., Rosario, L. E. De la Cruz, Ramírez, J. Roldán, León, J. P. Tirapu, Navarro-Guillamón, L., Cordovilla-Guardia, S., Iglesias-Santiago, A., Guerrero-López, F., Fernández-Mondéjar, E., Vidal, A., Perez, M., Juez, A., Arias, N., Colino, L., Perez, J. L., Pérez, H., Calpe, P., Alcala, M. A., Robaglia, D., Perez, C., Lan, S. K., Cunha, M. M., Moreira, T., Santos, F., Lafuente, E., Fernandes, M. J., Silva, J. G., Echeverría, J. G. Armando, Podlepich, V., Sokolova, E., Alexandrova, E., Lapteva, K., Shuinotsuka, C., Rabello, L., Vianna, G., Reis, A., Cairus, C., Salluh, J., Bozza, F., Torres, J. C. Barrios, Araujo, N. J. Fernández, García-Olivares, P., Keough, E., Dalorzo, M., Tang, L. K., De Sousa, I., Díaz, M., Marcos-Zambrano, L. J., Guerrero, J. E., Gomez, S. E. Zamora, Lopez, G. D. Hernandez, Cuellar, A. I. Vazquez, Nieto, O. R. Perez, Gonzalez, J. A. Castanon, Bhasin, D., Rai, S., Singh, H., Gupta, O., Bhattal, M. K., Sampley, S., Sekhri, K., Nandha, R., Aliaga, F. A., Olivares, F., Appiani, F., Farias, P., Alberto, F., Hernández, A., Pons, S., Sonneville, R., Bouadma, L., Neuville, M., Mariotte, E., Radjou, A., Lebut, J., Chemam, S., Voiriot, G., Dilly, M. P., Mourvillier, B., Dorent, R., Nataf, P., Wolff, M., Timsit, J. F., Ediboglu, O., Ataman, S., Ozkarakas, H., Kirakli, C., Vakalos, A., Avramidis, V., Obukhova, O., Kurmukov, I. A., Kashiya, S., Golovnya, E., Baikova, V. N., Ageeva, T., Haritydi, T., Kulaga, E. V., Rios-Toro, J. J., Lopez-Caler, C., Rodriguez-Fernandez, S., Sanchez-Orézzoli, M. Gomez, Martin-Gallardo, F., Nikhilesh, J., Joshi, V., Villarreal, E., Ruiz, J., Gordon, M., Quinza, A., Gimenez, J., Piñol, M., Castellanos, A., Ramirez, P., Jeon, Y. D., Jeong, W. Y., Kim, M. H., Jeong, I. Y., Ahn, M. Y., Ahn, J. Y., Han, S. H., Choi, J. Y., Song, Y. G., Kim, J. M., Ku, N. S., Shah, H., Kellner, F., Rezai, F., Mistry, N., Yodice, P., Ovnanian, V., Fless, K., Handler, E., Alejos, R. Martínez, Romeu, J. D. Martí, Antón, D. González, Quinart, A., Martí, A. Torres, Llaurado-Serra, M., Lobo-Civico, A., Ventura-Rosado, A., Piñol-Tena, A., Pi-Guerrero, M., Paños-Espinosa, C., Peralvo-Bernat, M., Marine-Vidal, J., Gonzalez-Engroba, R., Montesinos-Cerro, N., Treso-Geira, M., Valeiras-Valero, A., Martinez-Reyes, L., Sandiumenge, A., Jimenez-Herrera, M. F., Helyar, S., Riozzi, P., Noon, A., Hallows, G., Cotton, H., Keep, J., Hopkins, P. A., Taggu, A., Renuka, S., Sampath, S., Rood, P. J. T., Frenzel, T., Verhage, R., Bonn, M., Pickkers, P., van der Hoeven, J. G., van den Boogaard, M., Corradi, F., Melnyk, L., Moggia, F., Pienovi, R., Adriano, G., Brusasco, C., Mariotti, L., Lattuada, M., Bloomer, M. J., Coombs, M., Ranse, K., Endacott, R., Maertens, B., Blot, K., Blot, S., Amerongen, M. P. van Nieuw, van der Heiden, E. S., Twisk, J. W. R., Girbes, A. R. J., Spijkstra, J. J., Bell, C., Peters, K., Feehan, A., Churchill, K., Hawkins, K., Brook, R., Paver, N., Maistry, N., van Wijk, A., Rouw, N., van Galen, T., Evelein-Brugman, S., Krishna, B., Putzu, A., Fang, M., Berto, M. Boscolo, Belletti, A., Cassina, T., Cabrini, L., Mistry, M., Alhamdi, Y., Welters, I., Abrams, S. T., Toh, C. H., Han, H. S., Gil, E. M., Lee, D. S., Park, C. M., Winder-Rhodes, S., Lotay, R., Doyle, J., Ke, M. W., Huang, W. C., Chiang, C. H., Hung, W. T., Cheng, C. C., Lin, K. C., Lin, S. C., Chiou, K. R., Wann, S. R., Shu, C. W., Kang, P. L., Mar, G. Y., Liu, C. P., Dubó, S., Aquevedo, A., Jibaja, M., Berrutti, D., Labra, C., Lagos, R., García, M. F., Ramirez, V., Tobar, M., Picoita, F., Peláez, C., Carpio, D., Alegría, L., Hidalgo, C., Godoy, K., Bakker, J., Hernández, G., Sadamoto, Y., Katabami, K., Wada, T., Ono, Y., Maekawa, K., Hayakawa, M., Sawamura, A., Gando, S., Marin-Mateos, H., Perez-Vela, J. L., Garcia-Gigorro, R., Peiretti, M. A. Corres, Lopez-Gude, M. 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J., Revuelto-Rey, J., Aldabo-Pallas, T., Correa-Chamorro, E., Gallego-Corpa, A. I., Granados, P. Ruiz del Portal-Ruiz, Faivre, V., Wildenberg, L., Huot, B., Lukaszewicz, A. C., Simsir, M., Mengelle, C., Payen, D., Sanz, N. Martinez, de la Fuente, M. Valdivia, Almudena, P. Matía, Abellán, A. Navarro, Muñoz, J. J. Rubio, Abellan, A. Naharro, Lucendo, M. A. Perez, Perez, L. Perez, Dominguez, J. Palamidessi, Rivas, R. Fernandez, Villamizar, P. Rodriguez, Wee, S., Ong, C., Lau, Y. H., Wong, Y., Olea-Jiménez, V., Mora-Ordóñez, J. M., Muñoz-Muñoz, J. L., Vallejo-Báez, J., Daga-Ruiz, D., Lebrón-Gallardo, M., Rialp, G., Raurich, J. M., Morán, I., Martín, M. C., Heras, G., Mas, A., Vallverdú, I., Hraiech, S., Bourenne, J., Guervilly, C., Forel, J. M., Adda, M., Sylla, P., Mouaci, A., Gainnier, M., Papazian, L., Bauer, P. R., Kumbamu, A., Wilson, M. E., Pannu, J. K., Egginton, J. S., Kashyap, R., Gajic, O., Yoshihiro, S., Sakuraya, M., Hirata, A., Kawamura, N., Tsutui, T., Yoshida, K., Hashimoto, Y., Chang, C. H., Hu, H. C., Chiu, L. C., Hung, C. Y., Li, S. H., Kao, K. C., Sibley, S., Drover, J., D’Arsigny, C., Parker, C., Howes, D., Moffatt, S., Erb, J., Ilan, R., Messenger, D., Ball, I., Harrison, M., Ridi, S., Andrade, A. H., Costa, R. C., Souza, V. A., Gonzalez, V., Amorim, V., Rolla, F., Filho, C. A. C. Abreu, Miranda, R., Atchasiri, S., Buranavanich, P., Wathanawatthu, T., Suwanpasu, S., Bureau, C., Rolland-Debord, C., Poitou, T., Clavel, M., Perbet, S., Kouatchet, A., Similowski, T., Demoule, A., Diaz, P., Nunes, J., Escórcio, S., Silva, G., Chaves, S., Jardim, M., Câmara, M., Fernandes, N., Duarte, R., Jardim, J. J., Pereira, C. A., Nóbrega, J. J., Chen, C. M., Lai, C. C., Cheng, K. C., Chou, W., Lee, S. J., Cha, Y. S., Lee, W. Y., Onodera, M., Nakataki, E., Oto, J., Imanaka, H., Nishimura, M., Khadjibaev, A., Sabirov, D., Rosstalnaya, A., Akalaev, R., Parpibaev, F., Antonucci, E., Rossini, P., Gandolfi, S., Montini, E., Orlando, S., van Nes, M., Karachi, F., Hanekom, S., Pereira, U. V., Parkin, M. S. W., Moore, M., Carvalho, K. V. Silva, Min, H. J., Kim, H. J., Choi, Y. Y., Lee, E. Y., Song, I., Kim, D. J., E, Y. Y., Kim, J. W., Park, J. S., Lee, J. H., Suh, J. W., Jo, Y. H., Ferrero-Calleja, J., Merino-Vega, D., González-Jiménez, A. I., Sigcha, M. Sigcha, Hernández-Tejedor, A., Martin-Vivas, A., Gabán-Díez, Á., Luna, R. Ruiz-de, De la Calle-Pedrosa, N., Temprano-Gómez, I., Afonso-Rivero, D., Pellin-Ariño, J. I., Algora-Weber, A., Fumis, R. R. L., Ferraz, A. B., Junior, J. M. Vieira, Kirca, H., Cakin, O., Unal, M., Mutlu, H., Ramazanoglu, A., Cengiz, M., Nicolini, E. A., Pelisson, F. G. F., Nunes, R. S., da Silva, S. L., Carreira, M. M., Bellissimo-Rodrigues, F., Ferez, M. A., Basile-Filho, A., Chao, H. C., Chen, L., Hravnak, M., Clermont, G., Pinsky, M., Dubrawski, A., Varas, J. Luján, Montero, R. Molina, Sánchez-Elvira, L. Alcázar, Díaz, P. Villa, Delgado, C. Pintado, Ruiz, B. Llorente, Guerrero, A. Pardo, Galache, J. A. Cambronero, Sherif, H., Hassanin, H., El Hossainy, R., Samy, W., Ly, H., David, H., Burtin, P., Charpentier, C., Barral, M., Courant, P., Fournel, E., Gaide-Chevronnay, L., Durand, M., Albaladejo, P., Payen, J. F., Chavanon, O., Ortiz, A. Blandino, Pozzebon, S., Fumagalli, F., Scala, S., Affatato, R., De Maglie, M., Zani, D., Novelli, D., Marra, C., Luciani, A., De Zani, D., Luini, M., Letizia, T., Pravettoni, D., Staszewsky, L., Belloli, A., Di Giancamillo, M., Scanziani, E., Kye, Y. C., Yu, K. M., Babini, G., Grassi, L., Reinikainen, M., Skrifvars, M., Kappler, F., Blobner, M., Schaller, S. J., Roasio, A., Costanzo, E., Cardellino, S., Fontana, V., Park, M., You, K. M., Ko, S. B., Beane, A., Thilakasiri, M. C. K. T., De Silva, A. P., Stephens, T., Sigera, C. S., Athapattu, P., Jayasinghe, S., Padeniya, A., Haniffa, R., Sáez, V. Chica, Ruiz-Ruano, R. de la Chica, González, A. Sánchez, Kunze-Szikszay, N., Wand, S., Klapsing, P., Wetz, A., Heyne, T., Schwerdtfeger, K., Troeltzsch, M., Bauer, M., Quintel, M., Moerer, O., Cook, D. J., Rutherford, W. B., Scales, D. C., Adhikari, N. K., Cuthbertson, B. H., Suzuki, T., Fushimi, K., Iwamoto, M., Nakagawa, S., Mendsaikhan, N., Begzjav, T., Lundeg, G., Dünser, M. W., Romero, D. González, Padilla, Y. Santana, Kleinpell, R., Chouris, I., Radu, V., Stougianni, M., Lavrentieva, A., Lagonidis, D., Price, R. D. T., Day, A., Arora, N., Henderson, M. A., Hickey, S., Costa, M. I. Almeida, Carvalho, J. P., Gomes, A. A., Mergulhão, P. J., Chan, K. K. C., Maghsoudi, B., Tabei, S. H., Sabetian, G., Tabatabaei, H. R., Akbarzadeh, A., Saigal, S., Pakhare, A., Joshi, R., Pattnaik, S. K., Ray, B., Rousseau, A. F., Michel, L., Bawin, M., Cavalier, E., Reginster, J. Y., Damas, P., Bruyere, O., Zhou, J. C., Cauwenberghs, H., De Backer, A., Neels, H., Deblier, I., Berghmans, J., Himpe, D., Barea-Mendoza, J. A., Portillo, I. Prieto, Fernández, M. Valiente, Gigorro, R. Garcia, Vela, J. L. Perez, Mateos, H. Marín, Alves, S. Chacón, Varas, G. Morales, Rodriguez-Biendicho, A., Carreño, E. Renes, González, J. C. Montejo, Yang, J. S., Lin, K. L., Choi, Y. J., Yoon, S. Z., Gordillo-Brenes, A., Fernandez-Zamora, M. D., Herruzo-Aviles, A., Garcia-Delgado, M., Hinojosa-Perez, R., Pascual, O. Agudo, Irazabal, J. M. Guergue, Pérez, A. González, Fernández, P. Alvarez, Amor, L. Lopéz, Albaiceta, G. Muñiz, Calvo, S. Aldunate, Spazzadeschi, A., Marrazzo, F., Gandola, A., Sciurti, R., Savi, C., Tseng, C. J., Bertini, P., De Sanctis, F., Guarracino, F., Baldassarri, R., Buitinck, S. H., van der Voort, P. H. J., Tsunano, Y., Izawa, M., Tane, N., Ghosh, S., Gupta, A., De Gasperi, A., Mazza, E., Limuti, R., Prosperi, M., Bissenova, N., Yergaliyeva, A., Talan, L., Yılmaz, G., Güven, G., Yoruk, F., Altıntas, N. D., Mukherjee, D. N., Agarwal, L. K., Mandal, K., Balsera, B., Martinez, M., Garcia, M., Castellana, D., Lopez, R., Barcenilla, F., Kaminsky, G. E., Carreño, R., Escribá, A., Fuentes, M., Gálvez, V., Del Olmo, R., Nieto, B., Vaquerizo, C., Alvarez, J., De la Torre, M. A., Torres, E., Bogossian, E., Nouer, S. Aranha, Salgado, D. Ribeiro, Jiménez, G. Jiménez, Vidal, M. Vallverdú, Gaite, F. Barcenilla, Martínez, M. Palomar, Doganci, M., Izdes, S., Besevli, S. Guzeldag, Alkan, A., Kayaaslan, B., Penichet, S. M. Marrero, López, M. A. De La Cal, Santana, S. Ruíz, Repessé, X., Artiguenave, M., Paktoris-Papine, S., Espinasse, F., Dinh, A., El Sayed, F., Charron, C., Géri, G., Vieillard-Baron, A., Dimitroulakis, K., Ferré, A., Guillot, M., Teboul, J. L., Lichtenstein, D., Mézière, G., Richard, C., Monnet, X., Prīdāne, S., Sabeļņikovs, O., Bianchi, I., Kondili, E., Psarologakis, C., Kokkini, S., Amargianitakis, V., Babalis, D., Chytas, A., Chouvarda, I., Vaporidi, K., Georgopoulos, D., Trapp, O., Kalenka, A., Karbing, D. S., Gioia, A., Moro, F., Corte, F. Dalla, Mauri, T., Rees, S. E., Petrova, M. V., Mohan, R., Butrov, A. V., Beeharry, S. D., Vatsik, M. V., Sakieva, F. I., Gobert, F., Fernandez, R., Labaune, M. A., Burle, J. F., Barbier, J., Vincent, B., Cleyet, M., Shinotsuka, C. Righy, Törnblom, S., Nisula, S., Vaara, S., Poukkanen, M., Andersson, S., Pesonen, E., Xie, Z., Liao, X., Kang, Y., Zhang, J., Kubota, K., Egi, M., Mizobuchi, S., Hegazy, S., El-Keraie, A., El Sayed, E., El Hamid, M. Abd, Rodrigues, N. J., Pereira, M., Godinho, I., Gameiro, J., Neves, M., Gouveia, J., e Silva, Z. Costa, Lopes, J. A., Mckinlay, J., Kostalas, M., Kooner, G., Dudas, G., Horton, A., Kerr, C., Karanjia, N., Creagh-Brown, B., Yamazaki, A., Ganuza, M. Sanz, Molina, J. A. Martinez, Martinez, F. Hidalgo, Freile, M. T. Chiquito, Fernandez, N. Garcia, Travieso, P. Medrano, Bandert, A., Frithiof, R., Lipcsey, M., Smekal, D., Schlaepfer, P., Durovray, J. D., Plouhinec, V., Chiappa, C., Bellomo, R., Schneider, A. G., Mitchell, S., Durrant, J., Street, H., Dunthorne, E., Shears, J., Caballero, C. Hernandez, Hutchison, R., Schwarze, S., Ghabina, S., Thompson, E., Prowle, J. R., Kirwan, C. J., Gonzalez, C. A., Pinto, J. L., Orozco, V., Patiño, J. A., Garcia, P. K., Contreras, K. M., Rodriguez, P., and Echeverri, J. E.
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- 2016
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17. Impact of empirical treatment recommendations from 2017 European guidelines for nosocomial pneumonia.
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Calabretta D, Cilloniz C, Gabarrus A, Motos A, Galli F, Ferrer M, Fernandez-Barat L, Palomeque A, Mistraletti G, Panigada M, Pitart C, Espasa M, Martin-Loeches I, and Torres A
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- 2024
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18. Clinical Outcomes of Critical COVID-19 in HIV-Infected Adults: A Propensity Score Matched Analysis.
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Cilloniz C, Motos A, Canseco J, Peñasco Y, Ricart P, Abril E, García JMG, Ortiz AB, Mateo NG, Sánchez-Miralles Á, Franco N, Riera J, Ferrer R, Bustamante-Munguira E, Caballero J, Gándara AM, Sancho S, Masclans JR, Urrelo-Cerrón L, Carbonell N, Socías L, Barberà C, Lorente JA, Rodríguez ÓP, Menéndez R, de Gonzalo-Calvo D, Ceccato A, Fernandez-Barat L, Garcia-Gasulla D, Gabarrus A, Garcia-Vidal C, Moreno A, Barbé F, Miro JM, and Torres A
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- Humans, Adult, Propensity Score, Retrospective Studies, COVID-19 complications, HIV Infections complications, HIV Infections drug therapy, HIV Infections epidemiology
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- 2023
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19. Low anti-SARS-CoV-2 S antibody levels predict increased mortality and dissemination of viral components in the blood of critical COVID-19 patients.
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Martin-Vicente M, Almansa R, Martínez I, Tedim AP, Bustamante E, Tamayo L, Aldecoa C, Gómez JM, Renedo G, Berezo JÁ, Cedeño JA, Mamolar N, García Olivares P, Herrán-Monge R, Cicuendez R, Enríquez P, Ortega A, Jorge N, Doncel C, de la Fuente A, Bustamante-Munguira J, Muñoz-Gómez MJ, González-Rivera M, Puertas C, Más V, Vázquez M, Pérez-García F, Rico-Feijoo J, Martín S, Motos A, Fernandez-Barat L, Eiros JM, Dominguez-Gil M, Ferrer R, Barbé F, Trapiello W, Kelvin DJ, Bermejo-Martin JF, Resino S, and Torres A
- Subjects
- Critical Illness, Humans, RNA, Viral blood, SARS-CoV-2, Antibodies, Viral blood, Antigens, Viral blood, COVID-19 immunology, COVID-19 mortality
- Abstract
Background: Anti-SARS-CoV-2 S antibodies prevent viral replication. Critically ill COVID-19 patients show viral material in plasma, associated with a dysregulated host response. If these antibodies influence survival and viral dissemination in ICU-COVID patients is unknown., Patients/methods: We studied the impact of anti-SARS-CoV-2 S antibodies levels on survival, viral RNA-load in plasma, and N-antigenaemia in 92 COVID-19 patients over ICU admission., Results: Frequency of N-antigenaemia was >2.5-fold higher in absence of antibodies. Antibodies correlated inversely with viral RNA-load in plasma, representing a protective factor against mortality (adjusted HR [CI 95%], p): (S IgM [AUC ≥ 60]: 0.44 [0.22; 0.88], 0.020); (S IgG [AUC ≥ 237]: 0.31 [0.16; 0.61], <0.001). Viral RNA-load in plasma and N-antigenaemia predicted increased mortality: (N1-viral load [≥2.156 copies/ml]: 2.25 [1.16; 4.36], 0.016); (N-antigenaemia: 2.45 [1.27; 4.69], 0.007)., Conclusions: Low anti-SARS-CoV-2 S antibody levels predict mortality in critical COVID-19. Our findings support that these antibodies contribute to prevent systemic dissemination of SARS-CoV-2., (© 2021 The Association for the Publication of the Journal of Internal Medicine.)
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- 2022
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20. Development and characterization of a new swine model of invasive pneumococcal pneumonia.
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Amaro R, Li Bassi G, Motos A, Fernandez-Barat L, Aguilera Xiol E, Rigol M, Frigola G, Travierso C, Bobi J, Pagliara F, Carbonara M, Comaru T, Chiurazzi C, Yang M, Yang H, Arrieta M, Marti JD, De Rosa F, Saco MA, Rinaudo M, Terraneo S, Schultz MJ, Nicolau DP, Artigas A, Ramirez J, and Torres A
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- Animals, Anti-Bacterial Agents therapeutic use, Drug Resistance, Bacterial, Humans, Macrolides pharmacology, Streptococcus pneumoniae, Swine, Pneumonia, Pneumococcal drug therapy, Pneumonia, Pneumococcal veterinary
- Abstract
Streptococcus pneumoniae is the most common microbial cause of community-acquired pneumonia. Currently, there are no available models of severe pneumococcal pneumonia in mechanically ventilated animals to mimic clinical conditions of critically ill patients. We studied endogenous pulmonary flora in 4 healthy pigs and in an additional 10 pigs in which we intra-bronchially instilled S. pneumoniae serotype 19 A, characterized by its resistance to penicillin, macrolides and tetracyclines. The pigs underwent ventilation for 72 h. All pigs that were not challenged with S. pneumoniae completed the 72-h study, whereas 30% of infected pigs did not. At 24 h, we clinically confirmed pneumonia in the infected pigs; upon necropsy, we sampled lung tissue for microbiological/histological confirmation of pneumococcal pneumonia. In control pigs, Streptococcus suis and Staphylococcus aureus were the most commonly encountered pathogens, and their lung tissue mean ± s.e.m. concentration was 7.94 ± 20 c.f.u./g. In infected pigs, S. pneumoniae was found in the lungs of all pigs (mean ± s.e.m. pulmonary concentration of 1.26 × 10
5 ± 2 × 102 c.f.u./g). Bacteremia was found in 50% of infected pigs. Pneumococcal pneumonia was confirmed in all infected pigs at 24 h. Pneumonia was associated with thrombocytopenia, an increase in prothrombin time, cardiac output and vasopressor dependency index and a decrease in systemic vascular resistance. Upon necropsy, microbiological/histological pneumococcal pneumonia was confirmed in 8 of 10 pigs. We have therefore developed a novel model of penicillin- and macrolide-resistant pneumococcal pneumonia in mechanically ventilated pigs with bacteremia and severe hemodynamic compromise. The model could prove valuable for appraising the pathogenesis of pneumococcal pneumonia, the effects associated with macrolide resistance and the outcomes related to the use of new diagnostic strategies and antibiotic or complementary therapies., (© 2021. The Author(s), under exclusive licence to Springer Nature America, Inc.)- Published
- 2021
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21. [CIBERESUCICOVID: A strategic project for a better understanding and clinical management of COVID-19 in critical patients].
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Torres A, Arguimbau M, Bermejo-Martín J, Campo R, Ceccato A, Fernandez-Barat L, Ferrer R, Jarillo N, Lorente-Balanza JÁ, Menéndez R, Motos A, Muñoz J, Peñuelas Rodríguez Ó, Pérez R, Riera J, Rodríguez A, Sánchez M, and Barbe F
- Published
- 2021
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22. Short-Term Effects of Appropriate Empirical Antimicrobial Treatment with Ceftolozane/Tazobactam in a Swine Model of Nosocomial Pneumonia.
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Motos A, Li Bassi G, Pagliara F, Fernandez-Barat L, Yang H, Aguilera Xiol E, Senussi T, Idone FA, Travierso C, Chiurazzi C, Amaro R, Yang M, Bobi J, Rigol M, Nicolau DP, Frigola G, Cabrera R, Ramirez J, Pelosi P, Blasi F, Antonelli M, Artigas A, Vila J, Kollef M, and Torres A
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- Animals, Anti-Bacterial Agents pharmacology, Anti-Bacterial Agents therapeutic use, Cephalosporins pharmacology, Cephalosporins therapeutic use, Drug Resistance, Multiple, Bacterial, Microbial Sensitivity Tests, Penicillanic Acid pharmacology, Penicillanic Acid therapeutic use, Pseudomonas aeruginosa, Swine, Tazobactam pharmacology, Tazobactam therapeutic use, Anti-Infective Agents pharmacology, Cross Infection drug therapy, Healthcare-Associated Pneumonia, Pseudomonas Infections drug therapy
- Abstract
The rising frequency of multidrug-resistant and extensively drug-resistant (MDR/XDR) pathogens is making more frequent the inappropriate empirical antimicrobial therapy (IEAT) in nosocomial pneumonia, which is associated with increased mortality. We aim to determine the short-term benefits of appropriate empirical antimicrobial treatment (AEAT) with ceftolozane/tazobactam (C/T) compared with IEAT with piperacillin/tazobactam (TZP) in MDR Pseudomonas aeruginosa pneumonia. Twenty-one pigs with pneumonia caused by an XDR P. aeruginosa strain (susceptible to C/T but resistant to TZP) were ventilated for up to 72 h. Twenty-four hours after bacterial challenge, animals were randomized to receive 2-day treatment with either intravenous saline (untreated) or 25 to 50 mg of C/T per kg body weight (AEAT) or 200 to 225 mg of TZP per kg (IEAT) every 8 h. The primary outcome was the P. aeruginosa burden in lung tissue and the histopathology injury. P. aeruginosa burden in tracheal secretions and bronchoalveolar lavage (BAL) fluid, the development of antibiotic resistance, and inflammatory markers were secondary outcomes. Overall, P. aeruginosa lung burden was 5.30 (range, 4.00 to 6.30), 4.04 (3.64 to 4.51), and 4.04 (3.05 to 4.88) log
10 CFU/g in the untreated, AEAT, and IEAT groups, respectively ( P = 0.299), without histopathological differences ( P = 0.556). In contrast, in tracheal secretions ( P < 0.001) and BAL fluid ( P = 0.002), bactericidal efficacy was higher in the AEAT group. An increased MIC to TZP was found in 3 animals, while resistance to C/T did not develop. Interleukin-1β (IL-1β) was significantly downregulated by AEAT in comparison to other groups ( P = 0.031). In a mechanically ventilated swine model of XDR P. aeruginosa pneumonia, appropriate initial treatment with C/T decreased respiratory secretions' bacterial burden, prevented development of resistance, achieved the pharmacodynamic target, and may have reduced systemic inflammation. However, after only 2 days of treatment, P. aeruginosa tissue concentrations were moderately affected., (Copyright © 2021 American Society for Microbiology.)- Published
- 2021
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23. Viral RNA load in plasma is associated with critical illness and a dysregulated host response in COVID-19.
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Bermejo-Martin JF, González-Rivera M, Almansa R, Micheloud D, Tedim AP, Domínguez-Gil M, Resino S, Martín-Fernández M, Ryan Murua P, Pérez-García F, Tamayo L, Lopez-Izquierdo R, Bustamante E, Aldecoa C, Gómez JM, Rico-Feijoo J, Orduña A, Méndez R, Fernández Natal I, Megías G, González-Estecha M, Carriedo D, Doncel C, Jorge N, Ortega A, de la Fuente A, Del Campo F, Fernández-Ratero JA, Trapiello W, González-Jiménez P, Ruiz G, Kelvin AA, Ostadgavahi AT, Oneizat R, Ruiz LM, Miguéns I, Gargallo E, Muñoz I, Pelegrin S, Martín S, García Olivares P, Cedeño JA, Ruiz Albi T, Puertas C, Berezo JÁ, Renedo G, Herrán R, Bustamante-Munguira J, Enríquez P, Cicuendez R, Blanco J, Abadia J, Gómez Barquero J, Mamolar N, Blanca-López N, Valdivia LJ, Fernández Caso B, Mantecón MÁ, Motos A, Fernandez-Barat L, Ferrer R, Barbé F, Torres A, Menéndez R, Eiros JM, and Kelvin DJ
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- Adult, Aged, Biomarkers analysis, Biomarkers blood, COVID-19 blood, Chi-Square Distribution, Critical Illness, Female, Humans, Male, Middle Aged, Multivariate Analysis, Polymerase Chain Reaction methods, RNA, Viral blood, Statistics, Nonparametric, COVID-19 complications, RNA, Viral analysis, Viral Load immunology
- Abstract
Background: COVID-19 can course with respiratory and extrapulmonary disease. SARS-CoV-2 RNA is detected in respiratory samples but also in blood, stool and urine. Severe COVID-19 is characterized by a dysregulated host response to this virus. We studied whether viral RNAemia or viral RNA load in plasma is associated with severe COVID-19 and also to this dysregulated response., Methods: A total of 250 patients with COVID-19 were recruited (50 outpatients, 100 hospitalized ward patients and 100 critically ill). Viral RNA detection and quantification in plasma was performed using droplet digital PCR, targeting the N1 and N2 regions of the SARS-CoV-2 nucleoprotein gene. The association between SARS-CoV-2 RNAemia and viral RNA load in plasma with severity was evaluated by multivariate logistic regression. Correlations between viral RNA load and biomarkers evidencing dysregulation of host response were evaluated by calculating the Spearman correlation coefficients., Results: The frequency of viral RNAemia was higher in the critically ill patients (78%) compared to ward patients (27%) and outpatients (2%) (p < 0.001). Critical patients had higher viral RNA loads in plasma than non-critically ill patients, with non-survivors showing the highest values. When outpatients and ward patients were compared, viral RNAemia did not show significant associations in the multivariate analysis. In contrast, when ward patients were compared with ICU patients, both viral RNAemia and viral RNA load in plasma were associated with critical illness (OR [CI 95%], p): RNAemia (3.92 [1.183-12.968], 0.025), viral RNA load (N1) (1.962 [1.244-3.096], 0.004); viral RNA load (N2) (2.229 [1.382-3.595], 0.001). Viral RNA load in plasma correlated with higher levels of chemokines (CXCL10, CCL2), biomarkers indicative of a systemic inflammatory response (IL-6, CRP, ferritin), activation of NK cells (IL-15), endothelial dysfunction (VCAM-1, angiopoietin-2, ICAM-1), coagulation activation (D-Dimer and INR), tissue damage (LDH, GPT), neutrophil response (neutrophils counts, myeloperoxidase, GM-CSF) and immunodepression (PD-L1, IL-10, lymphopenia and monocytopenia)., Conclusions: SARS-CoV-2 RNAemia and viral RNA load in plasma are associated with critical illness in COVID-19. Viral RNA load in plasma correlates with key signatures of dysregulated host responses, suggesting a major role of uncontrolled viral replication in the pathogenesis of this disease.
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- 2020
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24. Aetiological diagnosis in new adult outpatients with bronchiectasis:role of predictors derived from real life experience.
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Ielpo A, Crisafulli E, Alcaraz-Serrano V, Gabarrús A, Oscanoa P, Scioscia G, Fernandez-Barat L, Cilloniz C, Amaro R, and Torres A
- Subjects
- Adult, Aged, Aged, 80 and over, Asthma, Female, Humans, Male, Middle Aged, Outpatients, Pneumonia, Predictive Value of Tests, Prospective Studies, Pulmonary Disease, Chronic Obstructive, Bronchiectasis diagnosis, Bronchiectasis etiology, Diagnostic Techniques, Respiratory System
- Abstract
Background: In adult patients with bronchiectasis (BE) the identification of the underlying aetiology may be difficult. In a new patient with BE the performance of a panel of tests is recommended, even though this practice may be expensive and the level of evidence supporting is low. We aimed to identify a panel of variables able to predict the aetiological diagnosis of BE., Methods: Our prospective study derived from our real-life experience on the management of adult stable BE outpatients. We recorded variables concerning clinical, radiological, microbiological and laboratory features. We identified five groups of aetiological diagnosis of BE (idiopathic, post-infective, COPD, asthma and non-common diseases [immunodeficiency or other rare conditions]). Multivariate models were used to identify predictors of each aetiological diagnosis. The suitability of performing a specific test for the diagnosis was also considered., Results: We enrolled 354 patients with a new diagnosis of BE. Patients with different aetiological causes differed significantly with regard to age, sex, smoking habit, comorbidities, dyspnoea perception, airflow obstruction and severity scores. Various predictors were assessed, including sex, previous respiratory infections, diffuse localization of BE, risk scores, and laboratory variables (sodium and eosinophils). The levels of autoantibodies or immunoglobulins were reserved for the diagnosis of non-common disease., Conclusion: Our research confirms that some predictors are specific for the aetiological diagnosis of BE. The possibility of integrating this information may represent a useful tool for the diagnosis. The execution of certain specific tests should be reserved for patients with a non-common disease., (Copyright © 2020 Elsevier Ltd. All rights reserved.)
- Published
- 2020
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25. SARS-CoV-2-induced Acute Respiratory Distress Syndrome: Pulmonary Mechanics and Gas-Exchange Abnormalities.
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Barbeta E, Motos A, Torres A, Ceccato A, Ferrer M, Cilloniz C, Bueno L, Badia JR, Castro P, Ferrando C, Andrea R, Castellà M, Fernández J, Soriano A, Mellado R, López-Aladid R, Yang H, Yang M, Fernandez-Barat L, Catalina Palomeque A, Vollmer I, and Nicolás JM
- Subjects
- Aged, COVID-19, Carbon Dioxide metabolism, Coronavirus Infections epidemiology, Female, Humans, Male, Middle Aged, Oxygen metabolism, Pandemics, Pneumonia, Viral epidemiology, Respiratory Distress Syndrome etiology, SARS-CoV-2, Betacoronavirus, Coronavirus Infections complications, Lung physiopathology, Pneumonia, Viral complications, Pulmonary Gas Exchange physiology, Respiratory Distress Syndrome physiopathology, Respiratory Mechanics physiology
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- 2020
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26. Systemic Inflammation during and after Bronchiectasis Exacerbations: Impact of Pseudomonas aeruginosa .
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Menéndez R, Méndez R, Amara-Elori I, Reyes S, Montull B, Feced L, Alonso R, Amaro R, Alcaraz V, Fernandez-Barat L, and Torres A
- Abstract
Bronchiectasis is a chronic structural disease associated with exacerbations that provoke systemic inflammation. We aimed to evaluate the systemic acute proinflammatory cytokine and its biomarker profiles during and after exacerbations and its relationship with the severity of episode, microbiological findings, and the bronchiectasis severity index. This prospective observational study compared exacerbation and stable groups. Cytokine (interleukins (IL)-17a, IL-1β, IL-6, IL 8; tumor necrosis factor-alpha (α)) and high-sensitivity C-reactive protein (hsCRP) levels were determined by multiplex analysis on days 1, 5, 30, and 60 in the exacerbation group and on day 1 in the stable group. We recruited 165 patients with exacerbations, of which 93 were severe (hospitalized). Proinflammatory systemic IL-17a, IL-1β, IL-8, and tumor necrosis factor-α levels increased similarly on days 1 and 5 in severe and non-severe episodes, but on day 30, IL-17a, IL-8, and IL-6 levels were only increased for severe exacerbations. The highest IL-17a level occurred in patients with chronic plus the acute isolation of Pseudomonas aeruginosa . At 30 days, severe exacerbations were independently associated with higher levels of IL-17 (Odds ratio (OR) 4.58), IL-6 (OR 4.89), IL-8 (OR 3.08), and hsCRP (OR 6.7), adjusted for age, the bronchiectasis severity index, and treatment duration. Exacerbations in patients with chronic P. aeruginosa infection were associated with an increase in IL-17 and IL-6 at 30 days (ORs 7.47 and 3.44, respectively). Severe exacerbations elicit a higher systemic proinflammatory response that is sustained to day 30. Patients with chronic P. aeruginosa infection had impaired IL-17a reduction. IL-17a could be a useful target for measuring systemic inflammation.
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- 2020
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27. Short-Term Appraisal of the Effects and Safety of Manual Versus Ventilator Hyperinflation in an Animal Model of Severe Pneumonia.
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Li Bassi G, Martí JD, Comaru T, Aguilera-Xiol E, Rigol M, Ntoumenopoulos G, Terraneo S, De Rosa F, Rinaudo M, Fernandez-Barat L, Battaglini D, Meli A, Ferrer M, Pelosi P, Chiumello D, and Torres A
- Subjects
- Animals, Disease Models, Animal, Mucociliary Clearance, Pneumonia microbiology, Pneumonia therapy, Pseudomonas Infections therapy, Pulmonary Ventilation physiology, Respiratory Mechanics, Swine, Treatment Outcome, Insufflation methods, Pneumonia complications, Pseudomonas Infections physiopathology, Pulmonary Atelectasis etiology, Pulmonary Atelectasis prevention & control, Respiration, Artificial adverse effects, Respiration, Artificial methods
- Abstract
Background: In patients on mechanical ventilation, lung hyperinflation is often performed to reverse atelectasis and clear retained mucus. We evaluated the effects of manual hyperinflation and ventilator hyperinflation on mucus clearance, gas exchange, pulmonary mechanics, and hemodynamics., Methods: Six mechanically ventilated pigs with severe Pseudomonas aeruginosa pneumonia randomly received either 12 manual hyperinflation breaths over a period of 2 min (through a gradual manual compression of a resuscitation bag within 4 s to achieve 40 cm H
2 O of airway pressure), or 12 ventilator hyperinflation over 2 min to achieve the same ventilatory end points as in manual hyperinflation. Mucus clearance rate was measured through fluoroscopic tracking of tracheal markers. Prior to each maneuver and 15 min thereafter, we assessed arterial and mixed gas exchange, pulmonary mechanics, and hemodynamics., Results: Both manual hyperinflation and ventilator hyperinflation significantly decreased inspiratory flow by approximately 16 L/min ( P < .001) and increased peak expiratory flow by roughly 44 L/min ( P < .001). The median (interquartile range) mucus clearance rate was 1.31 (0.84-2.30) prior to the interventions, and 0.70 (0.00-2.58) and 0.65 (0.45-1.47) during manual hyperinflation and ventilator hyperinflation, respectively ( P = .09). Hyperinflations, whether delivered manually or through the ventilator, did not significantly modify pulmonary or hemodynamic parameters., Conclusions: In an animal model of severe P. aeruginosa pneumonia, neither manual hyperinflation nor ventilator hyperinflation improved mucus clearance. If confirmed in comprehensive clinical experimentations, these findings should promote reappraisal of indications for both manual hyperinflation and ventilator hyperinflation as a therapeutic technique for mucus clearance and atelectasis reversal., (Copyright © 2019 by Daedalus Enterprises.)- Published
- 2019
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28. Nebulized Amikacin and Fosfomycin for Severe Pseudomonas aeruginosa Pneumonia: An Experimental Study.
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Li Bassi G, Motos A, Fernandez-Barat L, Aguilera Xiol E, Chiurazzi C, Senussi T, Saco MA, Fuster C, Carbonara M, Bobi J, Amaro R, De Rosa F, Comaru T, Yang H, Ranzani OT, Marti JD, Rinaudo M, Comino Trinidad O, Rigol M, Bringué J, Ramirez J, Nicolau DP, Pelosi P, Antonelli M, Blasi F, Artigas A, Montgomery AB, and Torres A
- Subjects
- Administration, Inhalation, Administration, Intravenous, Amikacin pharmacology, Animals, Anti-Bacterial Agents pharmacology, Bacterial Load drug effects, Bronchoalveolar Lavage Fluid microbiology, Disease Models, Animal, Drug Resistance, Bacterial, Drug Therapy, Combination, Female, Fosfomycin pharmacology, Lung microbiology, Lung pathology, Meropenem pharmacology, Nebulizers and Vaporizers, Pneumonia microbiology, Pneumonia pathology, Prospective Studies, Pseudomonas Infections complications, Random Allocation, Swine, Trachea metabolism, Trachea microbiology, Amikacin administration & dosage, Anti-Bacterial Agents administration & dosage, Fosfomycin administration & dosage, Meropenem administration & dosage, Pneumonia drug therapy, Pseudomonas Infections drug therapy, Pseudomonas aeruginosa drug effects
- Abstract
Objectives: Latest trials failed to confirm merits of nebulized amikacin for critically ill patients with nosocomial pneumonia. We studied various nebulized and IV antibiotic regimens in a porcine model of severe Pseudomonas aeruginosa pneumonia, resistant to amikacin, fosfomycin, and susceptible to meropenem., Design: Prospective randomized animal study., Setting: Animal Research, University of Barcelona, Spain., Subjects: Thirty female pigs., Interventions: The animals were randomized to receive nebulized saline solution (CONTROL); nebulized amikacin every 6 hours; nebulized fosfomycin every 6 hours; IV meropenem alone every 8 hours; nebulized amikacin and fosfomycin every 6 hours; amikacin and fosfomycin every 6 hours, with IV meropenem every 8 hours. Nebulization was performed through a vibrating mesh nebulizer. The primary outcome was lung tissue bacterial concentration. Secondary outcomes were tracheal secretions P. aeruginosa concentration, clinical variables, lung histology, and development of meropenem resistance., Measurements and Main Results: We included five animals into each group. Lung P. aeruginosa burden varied among groups (p < 0.001). In particular, IV meropenem and amikacin and fosfomycin + IV meropenem groups presented lower P. aeruginosa concentrations versus amikacin and fosfomycin, amikacin, CONTROL, and fosfomycin groups (p < 0.05), without significant difference between these two groups undergoing IV meropenem treatment. The sole use of nebulized antibiotics resulted in dense P. aeruginosa accumulation at the edges of the interlobular septa. Amikacin, amikacin and fosfomycin, and amikacin and fosfomycin + IV meropenem effectively reduced P. aeruginosa in tracheal secretions (p < 0.001). Pathognomonic clinical variables of respiratory infection did not differ among groups. Resistance to meropenem increased in IV meropenem group versus amikacin and fosfomycin + meropenem (p = 0.004)., Conclusions: Our findings corroborate that amikacin and fosfomycin alone efficiently reduced P. aeruginosa in tracheal secretions, with negligible effects in pulmonary tissue. Combination of amikacin and fosfomycin with IV meropenem does not increase antipseudomonal pulmonary tissue activity, but it does reduce development of meropenem-resistant P. aeruginosa, in comparison with the sole use of IV meropenem. Our findings imply potential merits for preemptive use of nebulized antibiotics in order to reduce resistance to IV meropenem.
- Published
- 2019
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29. Tracheal tube biofilm removal through a novel closed-suctioning system: an experimental study.
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Aguilera Xiol E, Li Bassi G, Wyncoll D, Ntoumenopoulos G, Fernandez-Barat L, Marti JD, Comaru T, De Rosa F, Rigol M, Rinaudo M, Ferrer M, and Torres A
- Subjects
- Animals, Equipment Contamination prevention & control, Female, Microscopy, Confocal, Pneumonia, Bacterial prevention & control, Pneumonia, Bacterial transmission, Pseudomonas Infections prevention & control, Pseudomonas Infections transmission, Pseudomonas aeruginosa, Suction methods, Sus scrofa, Biofilms, Intubation, Intratracheal instrumentation, Pneumonia, Ventilator-Associated prevention & control, Prosthesis-Related Infections prevention & control
- Abstract
Background: Tracheal tube biofilm develops during mechanical ventilation. We compared a novel closed-suctioning system vs standard closed-suctioning system in the prevention of tracheal tube biofilm., Methods: Eighteen pigs, on mechanical ventilation for 76 h, with P. aeruginosa pneumonia were randomized to be tracheally suctioned via the KIMVENT* closed-suctioning system (control group) or a novel closed-suctioning system (treatment group), designed to remove tracheal tube biofilm through saline jets and an inflatable balloon. Upon autopsy, two tracheal tube hemi-sections were dissected for confocal and scanning electron microscopy. Biofilm area, maximal and minimal thickness were computed. Biofilm stage was assessed., Results: Sixteen animals were included in the final analysis. In the treatment and control group, the mean (sd) pulmonary burden was 3.34 (1.28) and 4.17 (1.09) log cfu gr(-1), respectively (P=0.18). Tracheal tube P. aeruginosa colonization was 5.6 (4.9-6.3) and 6.2 (5.6-6.9) cfu ml(-1) (median and interquartile range) in the treatment and control group, respectively (P=0.23). In the treatment group, median biofilm area was 3.65 (3.22-4.21) log10 μm2 compared with 4.49 (4.27-4.52) log10 μm2 in the control group (P=0.031). In the treatment and control groups, the maximal biofilm thickness was 48.3 (26.7-71.2) µm (median and interquartile range) and 88.8 (43.8-125.7) µm, respectively. The minimal thickness in the treatment and control group was 0.6 (0-4.0) µm and 23.7 (5.3-27.8) µm (P=0.040) (P=0.017). Earlier stages of biofilm development were found in the treatment group (P<0.001)., Conclusions: The novel CSS reduces biofilm accumulation within the tracheal tube. A clinical trial is required to confirm these findings and the impact on major outcomes., (© The Author 2015. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)
- Published
- 2015
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30. Endotracheal tube biofilm translocation in the lateral Trendelenburg position.
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Li Bassi G, Fernandez-Barat L, Saucedo L, Giunta V, Marti JD, Tavares Ranzani O, Aguilera Xiol E, Rigol M, Roca I, Muñoz L, Luque N, Esperatti M, Saco MA, Ramirez J, Vila J, Ferrer M, and Torres A
- Subjects
- Animals, Bronchitis microbiology, Lung microbiology, Microscopy, Confocal, Microscopy, Electron, Scanning, Models, Animal, Pneumonia, Ventilator-Associated prevention & control, Swine, Tracheitis microbiology, Bacterial Adhesion, Biofilms, Intubation, Intratracheal instrumentation, Patient Positioning
- Abstract
Introduction: Laboratory studies demonstrated that the lateral Trendelenburg position (LTP) is superior to the semirecumbent position (SRP) in the prevention of ventilator-associated pulmonary infections. We assessed whether the LTP could also prevent pulmonary colonization and infections caused by an endotracheal tube (ETT) biofilm., Methods: Eighteen pigs were intubated with ETTs colonized by Pseudomonas aeruginosa biofilm. Pigs were positioned in LTP and randomized to be on mechanical ventilatin (MV) up to 24 hour, 48 hour, 48 hour with acute lung injury (ALI) by oleic acid and 72 hour. Bacteriologic and microscopy studies confirmed presence of biofilm within the ETT. Upon autopsy, samples from the proximal and distal airways were excised for P.aeruginosa quantification. Ventilator-associated tracheobronchitis (VAT) was confirmed by bronchial tissue culture ≥3 log colony forming units per gram (cfu/g). In pulmonary lobes with gross findings of pneumonia, ventilator-associated pneumonia (VAP) was confirmed by lung tissue culture ≥3 log cfu/g., Results: P.aeruginosa colonized the internal lumen of 16 out of 18 ETTs (88.89%), and a mature biofilm was consistently present. P.aeruginosa colonization did not differ among groups, and was found in 23.6% of samples from the proximal airways, and in 7.1% from the distal bronchi (P = 0.001). Animals of the 24 hour group never developed respiratory infections, whereas 20%, 60% and 25% of the animals in group 48 hour, 48 hour-ALI and 72 hour developed P.aeruginosa VAT, respectively (P = 0.327). Nevertheless, VAP never developed., Conclusions: Our findings imply that during the course of invasive MV up to 72 hour, an ETT P.aeruginosa biofilm hastily colonizes the respiratory tract. Yet, the LTP compartmentalizes colonization and infection within the proximal airways and VAP never develops.
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- 2015
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31. A novel porcine model of ventilator-associated pneumonia caused by oropharyngeal challenge with Pseudomonas aeruginosa.
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Li Bassi G, Rigol M, Marti JD, Saucedo L, Ranzani OT, Roca I, Cabanas M, Muñoz L, Giunta V, Luque N, Rinaudo M, Esperatti M, Fernandez-Barat L, Ferrer M, Vila J, Ramirez J, and Torres A
- Subjects
- Animals, Female, Oropharynx microbiology, Pneumonia, Ventilator-Associated epidemiology, Pseudomonas Infections complications, Swine, Disease Models, Animal, Oropharynx pathology, Pneumonia, Ventilator-Associated microbiology, Pneumonia, Ventilator-Associated pathology, Pseudomonas Infections pathology, Pseudomonas aeruginosa pathogenicity
- Abstract
Background: Animal models of ventilator-associated pneumonia (VAP) in primates, sheep, and pigs differ in the underlying pulmonary injury, etiology, bacterial inoculation methods, and time to onset. The most common ovine and porcine models do not reproduce the primary pathogenic mechanism of the disease, through the aspiration of oropharyngeal pathogens, or the most prevalent human etiology. Herein the authors characterize a novel porcine model of VAP due to aspiration of oropharyngeal secretions colonized by Pseudomonas aeruginosa., Methods: Ten healthy pigs were intubated, positioned in anti-Trendelenburg, and mechanically ventilated for 72 h. Three animals did not receive bacterial challenge, whereas in seven animals, a P. aeruginosa suspension was instilled into the oropharynx. Tracheal aspirates were cultured and respiratory mechanics were recorded. On autopsy, lobar samples were obtained to corroborate VAP through microbiological and histological studies., Results: In animals not challenged, diverse bacterial colonization of the airways was found and monolobar VAP rarely developed. In animals with P. aeruginosa challenge, colonization of tracheal secretion increased up to 6.39 ± 0.34 log colony-forming unit (cfu)/ml (P < 0.001). VAP was confirmed in six of seven pigs, in 78% of the cases developed in the dependent lung segments (right medium and lower lobes, P = 0.032). The static respiratory system elastance worsened to 41.5 ± 5.8 cm H2O/l (P = 0.001)., Conclusions: The authors devised a VAP model caused by aspiration of oropharyngeal P. aeruginosa, a frequent causative pathogen of human VAP. The model also overcomes the practical and legislative limitations associated with the use of primates. The authors' model could be employed to study pathophysiologic mechanisms, as well as novel diagnostic/preventive strategies.
- Published
- 2014
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