Molecular mechanisms of beta-lactam resistance mediated by AmpC hyperproduction in Pseudomonas aeruginosa clinical strains.

ABSTRACT: The molecular mechanisms of beta-lactam resistance mediated by AmpC hyperproduction in natural strains of Pseudomonas aeruginosa were investigated in a collection of 10 isogenic, ceftazidime-susceptible and -resistant pairs of isolates, each sequentially recovered from a different intensive care unit patient treated with beta-lactams. All 10 ceftazidime-resistant mutants hyper-produced AmpC (beta-lactamase activities were 12- to 657-fold higher than those of the parent strains), but none of them harbored mutations in ampR or the ampC-ampR intergenic region. On the other hand, six of them harbored inactivating mutations in ampD: four contained frameshift mutations, one had a C-->T mutation, creating a premature stop codon, and finally, one had a large deletion, including the complete ampDE

SUBMITTER: Juan C 

PROVIDER: S-EPMC1280133 | biostudies-literature | 2005 Nov

REPOSITORIES: biostudies-literature