At least 30 extended-spectrum beta-lactamases (ESB) have emerged responsible for resistance to indigestible beta-lactams (C3G) since their discovery in West Germany in 1983. Most of them are produced by enterobacteria and essentially K. pneumoniae which appeared susceptible to oxyimino-beta-lactams. A double-disk test was useful to detect such nosocomial isolates of enterobacteria (urines, blood, wound, sputum cultures) mostly recovered from patients in intensive care units. These have spread through hospital and outbreaks were described. Because plasmid-encoded this resistance mechanism was spreading among enterobacteria with other resistance markers (e.g. netilmicin, amikacin). It seems highly likely that the use of newer antibiotics favors the appearance of ESB obtained by selection of mutated genes coding for penicillinases (TEM, SHV). Treatment including a beta-lactam is still possible because of the stability of some beta-lactams e.g. cefamycins, carbapenems and the sensitivity to beta-lactam inhibitors. Digestive selective decontamination may overcome outbreak.