Pseudomonas aeruginosa has an inducible, naturally occurring cephalosporinase that confers low-level resistance to aminopenicillins and narrow-spectrum cephalosporins such as cephalothin and cefoxitin (1). Resistance to extendedspectrum cephalosporins may arise from overexpression of this cephalosporinase, acquired beta-lactamases, or both (1). The acquired beta-lactamases may be either clavulanic-acid inhibited (mostly Ambler class A enzymes) or clavulanic-acid resistant (class B and class D enzymes) (2). The class A extended-spectrum beta-lactamases (ESBLs) may derive from narrow-spectrum beta-lactamases of TEM and SHV types, as extensively reported for Enterobacteriaceae and rarely for P. aeruginosa (2). Other class A enzymes reported in P. aeruginosa include PER-1, which we first identified as chromosomally located and which is widespread in P. aeruginosa isolates in Turkey (11% of the hospital isolates) (3,4). Lately, another class A ESBL integron-located gene, bla VEB-1 , has been identified from P. aeruginosa and enterobacterial isolates from Southeast Asia (5-7).
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Poirel et al. (2001) studied this question.
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