Antimicrobial resistance among 1991 isolates collected at 24 UK hospitals during late 1993 was surveyed. Three-hundred and seventy-two of the isolates were resistant, or had reduced susceptibility, to some or all of azlocillin, carbenicillin, ceftazidime, imipenem and meropenem, and the mechanisms underlying their behaviour were examined. Only 13 isolates produced secondary β-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 carbenicillin whereas those with OXA enzymes were less resistant to these penicillins. Chromosomal β-lactamase derepression was demonstrated in 54 isolates, most of which were resistant to ceftazidime and azlocillin although susceptible to carbenicillin and carbapenems. β-Lactamase-independent “intrinsic” resistance occurred in 277 isolates and is believed to reflect some combination of impermeability and efflux. Two forms were seen: The classical type, present in 195 isolates, gave carbenicillin resistance (MIC > 128 mg/L) and reduced susceptibility to ciprofloxacin and to all β-lactam agents except imipenem; a novel variant, seen in 82 isolates, affected only azlocillin, ceftazidime and, to a small extent, meropenem. Resistance to imipenem was largely dissociated from that to other β-lactam agents, and probably reflected loss of D2 porin, whereas resistance to meropenem was mostly associated with intrinsic resistance to penicillins and cephalosporins. Comparison of the present results with those of a similar study in 1982 revealed significant increases in the proportions of isolates with intrinsic resistance or stable derepression (p ≪0·01, x test). Isolates with secondary β-lactamases appeared significantly rarer than in 1982 (p ≪ 0·01, X test), but this comparison was distorted by outbreak strains.


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