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The majority of /3-lactam antibiotics have become increasingly ineffective therapeutic agents due to the rapid development of resistant strains^. Mechanismsresponsible for the development of resistance to /Mactams include (i) hydrolysis by /3-lactamases, (ii) creation of nonhydrolytic barriers by /?-lactamases, (iii) reduction in affinity of target proteins, and (iv) reduction in permeability2). For Gramnegative enteric bacteria, the emergence of resistance to broad-spectrum penicillins and jS-lactamase-stable cephalosporins occurs frequently3). The complexity of (3lactamase epidemiology has greatly increased with the emergence of extended-spectrum /3-lactamases (ESBLs) derived from plasmid-encoded TEM and SHV-type enzymes4). These /J-lactamases show greater specificity for /3-lactam antibiotics. /3-Lactamases are divided by their substrates into classes A, B, C and D. Whenan isolate produces two different classes of /3-lactamases, the genes coding for each /3lactamase are located separately on a plasmid and on a chromosome. For example, plasmid-encoded class A enzymes and chromosome-encoded class C enzymes are produced in Gram-negative bacteria. On the other hand, plasmid-encoded class B enzymes have been reported from Japan5). However, there are no reports of plasmids carrying the genes of two different classes of /Mactamases, such as class A and class B or class A and class D. pp.1135 1139

Presence of Genes for .BETA.-Lactamases of Two Different Classes on a Single Plasmid from a Clinical Isolate of Serrtia marcescens.