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In Vivo Resistance to Ceftolozane/Tazobactam in Pseudomonas aeruginosa Arising by AmpC- and Non-AmpC-Mediated Pathways

2018; Hindawi Publishing Corporation; Volume: 2018; Linguagem: Inglês

10.1155/2018/9095203

2090-6625

Erik Skoglund, Henrietta Abodakpi, Rafael Ríos, Lorena Díaz, Elsa De La Cadena, An Q Dinh, Javier Ardila, William R. Miller, José M. Munita, César A. Arias, Vincent H. Tam, Truc T. Tran,

Antimicrobial Resistance in Staphylococcus

Two pairs of ceftolozane/tazobactam susceptible/resistant P. aeruginosa were isolated from 2 patients after exposure to β -lactams. The genetic basis of ceftolozane/tazobactam resistance was evaluated, and β -lactam-resistant mechanisms were assessed by phenotypic assays. Whole genome sequencing identified mutations in AmpC including the mutation (V213A) and a deletion of 7 amino acids (P210–G216) in the Ω-loop. Phenotypic assays showed that ceftolozane/tazobactam resistance in the strain with AmpC V213A variant was associated with increased β -lactamase hydrolysis activity. On the other hand, the deletion of 7 amino acids in the Ω-loop of AmpC did not display enhanced β -lactamase activity. Resistance to ceftolozane/tazobactam in P. aeruginosa is associated with changes in AmpC; however, the apparent loss of β -lactamase activity in AmpC∆7 suggests that non-AmpC mechanisms could play an important role in resistance to β -lactam/ β -lactamase inhibitor combinations.