Pablo A Fraile-Ribot 1, Laura Zamorano 1, Rocío Orellana 1, Ester Del Barrio-Tofiño 1, Irina Sánchez-Diener 1, Sara Cortes-Lara 1, Carla López-Causapé 1, Gabriel Cabot 1, Germán Bou 3, Luis Martínez-Martínez 4, Antonio Oliver 2; GEMARA-SEIMC/REIPI Pseudomonas Study Group
1Servicio de Microbiología, Hospital Son Espases, Instituto de Investigación Sanitaria Illes Balears (IdISBa), Palma de Mallorca, Spain.
2Servicio de Microbiología, Hospital Son Espases, Instituto de Investigación Sanitaria Illes Balears (IdISBa), Palma de Mallorca, Spain laura.zamorano@ssib.es antonio.oliver@ssib.es.
3Servicio de Microbiología, Hospital Universitario La Coruña, Instituto Investigación Biomédica A Coruña (INIBIC), A Coruna, Spain.
3 Unidad de Gestión Clínica de Microbiología, Hospital Reina Sofía, Departamento de Microbiología, Universidad de Córdoba, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Cordoba, Spain.
Abstract:
Imipenem and imipenem-relebactam MICs were determined for 1,445 Pseudomonas aeruginosa clinical isolates and a large panel of isogenic mutants showing the most relevant mutation-driven β-lactam resistance mechanisms. Imipenem-relebactam showed the highest susceptibility rate (97.3%), followed by colistin and ceftolozane-tazobactam (both 94.6%). Imipenem-relebactam MICs remained ≤2 μg/ml in all 16 isogenic PAO1 mutants and in 8 pairs of extensively drug-resistant clinical strains that had developed resistance to ceftolozane-tazobactam and ceftazidime-avibactam due to mutations in OXA-10 or AmpC.
Antimicrob Agents Chemoter. 2020 Jan 27;64(2):e02165-19. doi: 10.1128/AAC.02165-19.
Link to Antimicrob Agents Chemoter