Leclercia adecarboxylata is an opportunistic human pathogen that phenotypically resembles Escherichia coli. The natural susceptibilities of 101 Leclercia strains to 70 antimicrobial agents were investigated. MICs were determined with a microdilution procedure in cation-adjusted Mueller-Hinton broth (all strains) and IsoSensitest broth (some strains). Natural susceptibility patterns were assessed using German (DIN) standards (when applicable). In addition, biochemical properties recommended for the phenotypic identification of L. adecarboxylata were evaluated, applying two commercially available identification systems for Enterobacteriaceae and seven conventional tests. L. adecarboxylata strains were naturally sensitive to tetracyclines, aminoglycosides, all but two beta-lactams, quinolones, folate pathway inhibitors, chloramphenicol, nitrofurantoin and azithromycin. They were naturally resistant to penicillin G, oxacillin, erythromycin, roxithromycin, clarithromycin, ketolides, lincosamides, streptogramins, linezolid, glycopeptides, rifampicin, fusidic acid and fosfomycin. There were only minor medium-dependent differences in susceptibility to most antibiotics. Lysine decarboxylase, malonate assimilation and acid production from arabitol and cellobiose, but not from adonitol and sorbitol, allowed definitive separation of L. adecarboxylata from E. coli. The results of this study form a database that can be applied to validate forthcoming antibiotic susceptibility tests of L. adecarboxylata, and might contribute to its reliable identification. Susceptibility patterns did not indicate obvious therapeutic difficulties for treatment of Leclercia infections. Special attention should be paid to biochemically aberrant leclerciae. Apart from biochemical features, fosfomycin susceptibility might be useful to differentiate between L. adecarboxylata and E. coli.

The natural susceptibility to 71 antibiotics of 104 Serratia strains of Serratia ficaria (n = 15), Serratia fonticola (n = 18), Serratia odorifera (n = 16), Serratia plymuthica (n = 32) and Serratia rubidaea (n = 23) was examined. MICs were determined using a microdilution procedure in IsoSensitest broth for all the strains and in cation-adjusted Mueller-Hinton broth for some strains. With few exceptions, all species tested were uniformly naturally resistant to penicillin G, oxacillin, cefazolin, cefuroxime, all tested macrolides, lincosamides, streptogramins, glycopeptides, fusidic acid and rifampicin, and naturally sensitive to several aminoglycosides, piperacillin, piperacillin/tazobactam, carbapenems, some cephalosporins, fluoroquinolones and folate-pathway inhibitors. Major species-related differences in natural susceptibility affecting clinical assessment criteria were seen with tetracyclines, some aminoglycosides, aminopenicillins, ticarcillin, cefaclor, loracarbef, cefoxitin, pipemidic acid, chloramphenicol, nitrofurantoin and fosfomycin. Differences in susceptibility dependent on the medium were seen with macrolides, tetracycline, fosfomycin and some beta-lactams. The natural antibiotic susceptibility patterns suggest novel species-specific mechanisms of antibiotic resistance. Uncharacterized species-specific aminoglycoside-modifying enzymes and multidrug efflux systems affecting tetracyclines, quinolones and chloramphenicol are probably responsible for some of the phenotypes observed. The natural amoxicillin sensitivity of several strains of some species combined with natural resistance to some narrow-spectrum cephalosporins indicate the expression of naturally occurring beta-lactamases with unique substrate profiles. beta-Lactamases of representative strains of each species were characterized phenotypically and genotypically. It was shown that all species expressed naturally occurring AmpC beta-lactamases and, with respect to S. fonticola, also a species-specific class A beta-lactamase. Inducibility of these enzymes was shown in all species with the exception of S. rubidaea and four of five strains of S. plymuthica.

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