Resistance of Pseudomonas species to beta-lactam antibiotics.
Resistance of Pseudomonas species to beta-lactam compounds involves both drug exclusion and hydrolytic inactivation. Exclusion is effected by a permeability barrier in the cell envelope, whereas hydrolysis is effected by beta-lactamases, encoded either by the chromosome or by R-plasmids. Chromosomally-mediated beta-lactamases are generally inducible and have a high activity against cephalosporins. They are virtually universally present in P. aeruginosa. Conversely, the generally infrequent R-plasmid-mediated beta-lactamases are constitutive, with substrate profiles specific to each enzyme type. Four Pseudomonas-specific R-plasmid-mediated beta-lactamases are responsible for high level resistance to carbenicillin. Resistance to carbenicillin may also be associated with isolates not possessing this type of beta-lactamase: the permeability barrier effect is probably highly significant in these isolates.
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D002875:Chromosomes / Q000502:physiology; D004352:Drug Resistance, Microbial; D004355:Drug Stability; D011549:Pseudomonas / Q000187:drug effects*; D011815:R Factors; D001618:beta-Lactamases / Q000235:genetics / Q000378:metabolism; D047090:beta-Lactams / Q000494:pharmacology
D000900:Anti-Bacterial Agents; D047090:beta-Lactams; D001618:beta-Lactamases