• José A Martínez, Esther Delgado, Sara Martí, Francesc Marco, Jordi Vila, Josep Mensa, Antoni Torres, Carles Codina, Antoni Trilla, Alex Soriano, Aitor Alquezar, Pedro Castro, and José M Nicolás.
• Department of Infectious Diseases, Hospital Clínic, IDIBAPS, University of Barcelona, Barcelona, Spain. jamarti@clinic.ub.es
• Intensive Care Med. 2009 Mar 1;35(3):439-47.

ObjectiveTo assess the role of antipseudomonal agents on Pseudomonas aeruginosa colonization and acquisition of resistance.DesignProspective cohort study.SettingTwo medical intensive care units.Patients And Participants346 patients admitted for >or= 48 h.InterventionAnalysis of data from an 8-month study comparing a mixing versus a cycling strategy of antibiotic use.Measurements And ResultsSurveillance cultures from nares, pharynx, rectum, and respiratory secretions were obtained thrice weekly. Acquisition of resistance was defined as the isolation, after 48 h of ICU stay, of an isolate resistant to a given antibiotic if culture of admission samples were either negative or positive for a susceptible isolate. Emergence of resistance refers to the conversion of a defined pulsotype from susceptible to non-susceptible. Forty-four (13%) patients acquired 52 strains of P. aeruginosa. Administration of piperacillin-tazobactam for >or= 3 days (OR 2.6, 95% CI 1.09-6.27) and use of amikacin for >or= 3 days (OR 2.6, 95% CI 1.04-6.7) were positively associated with acquisition of P. aeruginosa, whereas use of quinolones (OR 0.27, 95% CI 0.1-0.7) and antipseudomonal cephalosporins (OR 0.27, 95% CI 0.08-0.9) was protective. Exposure to quinolones and cephalosporins was not associated with the acquisition of resistance, whereas it was linked with usage of all other agents. Neither quinolones nor cephalosporins were a major determinant on the emergence of resistance to themselves, as resistance to these antibiotics developed at a similar frequency in non-exposed patients.ConclusionsIn critically ill patients, quinolones and antipseudomonal cephalosporins may prevent the acquisition of P. aeruginosa and may have a negligible influence on the acquisition and emergence of resistance.

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