Beta-lactamases still play an important part in medical bacteriology, as shown by the emergence, since 1983, of plasmid-mediated beta-lactamases with an enlarged spectrum (SHV-2, CTX-1, etc.). Such enzymes are only produced by enterobacteria and, more specifically, by Klebsiella pneumoniae. This phenomenon, described in Europe and in Africa, is certainly more widespread than it would appear, as some strains are now known to be less sensitive to third generation cephalosporins (MIC 1 to 4 mg/l). Despite differences in behaviour (cefotaximase and ceftazidimase phenotypes), resistance to amino-, carboxy- and ureido-penicillins is associated with reduced sensitivity or resistance to oxyimino beta-lactams (cefotaxime, ceftriaxone, ceftazidime, aztreonam), but cefamycins and imipenem are untouched. Being sensitive to enzyme inhibitors (e.g. clavulanic acid), these beta-lactamases can easily be detected and some infections (notably urinary tract infections) can probably be treated using these inhibitors. These enzymes show modified kinetic constants (better affinity and quicker hydrolysis) against penicillins, third generation aminothiazolimino-cephalosporins and aztreonam. The producing strains are mutants, with aminoacid 1 to 2 substitutions, of those which produce the usual plasmid-borne and transposable beta-lactamases (TEM or SHV). Because these beta-lactamases are plasmid-mediated, enzyme production mechanisms are spreading among enterobacteria species in relation to other resistance markers (tobramycin, netilmicin, amikacin). Strains which produce these new enzymes are mainly isolated from patients treated in intensive care units.