Antibiotic resistance of Pseudomonas species.
Pseudomonas species are highly versatile organisms with genetic and physiologic capabilities that allow them to flourish in environments hostile to most pathogenic bacteria. Within the lung of the patient with cystic fibrosis, exposed to a number of antimicrobial agents, highly resistant clones of Pseudomonas are selected. These may have acquired plasmid-mediated genes encoding a variety of beta-lactamases or aminoglycoside modifying enzymes. Frequently these resistance determinants are on transposable elements, facilitating their dissemination among the population of bacteria. Mutations in chromosomal genes can also occur, resulting in constitutive expression of normally repressed enzymes, such as the chromosomal cephalosporinase of Pseudomonas aeruginosa or Pseudomonas cepacia. These enzymes may confer resistance to the expanded-spectrum beta-lactam drugs. Decreased cellular permeability to the beta-lactams and the aminoglycosides also results in clinically significant antibiotic resistance. The development of new drugs with anti-Pseudomonas activity, beta-lactam agents and the quinolones, has improved the potential for effective chemotherapy but has not surpassed the potential of the organisms to develop resistance.
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D000617:Aminoglycosides / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D003550:Cystic Fibrosis / Q000150:complications; D004352:Drug Resistance, Microbial; D006801:Humans; D007769:Lactams; D009268:Nalidixic Acid / Q000031:analogs & derivatives; D011549:Pseudomonas / Q000187:drug effects*; D011552:Pseudomonas Infections / Q000150:complications / Q000188:drug therapy; D011804:Quinolines / Q000494:pharmacology
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D007769:Lactams; D011804:Quinolines; D009268:Nalidixic Acid