MECHANISMS OF RESISTANCE TO BETA-LACTAM ANTIBIOTICS AMONGST PSEUDOMONAS-AERUGINOSA ISOLATES COLLECTED IN THE UK IN 1993

Antimicrobial resistance among 1991 Pseudomonas aeruginosa isolates co llected at 24 UK hospitals during late 1993 was surveyed. Three-hundre d and seventy-two of the isolates were resistant, or had reduced susce ptibility, to some or all of azlocillin, carbenicillin, ceftazidime, i mipenem and meropenem, and the mechanisms underlying their behaviour w ere examined. Only 13 isolates produced secondary beta-lactamases: six possessed PSE-1 or PSE-4 enzymes and seven had novel OXA enzyme types . Those with PSE types were highly resistant to azlocillin and carbeni cillin whereas those with OXA enzymes were less resistant to these pen icillins. Chromosomal beta-lactamase derepression was demonstrated in 54 isolates, most of which were resistant to ceftazidime and azlocilli n although susceptible to carbenicillin and carbapenems. beta-Lactamas e-independent ''intrinsic'' resistance occurred in 277 isolates and is believed to reflect some combination of impermeability and efflux. Tw o forms were seen: the classical type, present in 195 isolates, gave c arbenicillin resistance (MIC > 128 mg/L) and reduced susceptibility to ciprofloxacin and to all beta-lactam agents except imipenem; a novel variant, seen in 82 isolates, affected only azlocillin, ceftazidime an d, to a small extent, meropenem. Resistance to imipenem was largely di ssociated from that to other beta-lactam agents, and probably reflecte d loss of D2 porin, whereas resistance to meropenem was mostly associa ted with intrinsic resistance to penicillins and cephalosporins. Compa rison of the present results with those of a similar study in 1982 rev ealed significant increases in the proportions of isolates with intrin sic resistance or stable derepression (p < 0.01, chi(2) test). Isolate s with secondary beta-lactamases appeared significantly rarer than in 1982 (p < 0.01, chi(2) test), but this comparison was distorted by out break strains.