| BackgroundSoon after introducing the clinical use of extended-spectrum cephalosporins,such as cefotaxime, ceftriaxone, ceftazidime, aztreonam and Cefpodoxime, extended-spectrum β -lactamase(ESBLs) were firstly isolated from Enterobacteriaceae in Europe. Then , in about 20 years, ESBLs were reported around the world. Its rates of detection increased year after year. The subtype of ESBLs went up gradually and have been found two hundred or so till April, 2005. ESBLs were produced by Gram-negative bacteria , such as Klebsiellae pneumoniae, Escherichia coli, Enterobacter cloacae, Acinetobacter sp. and Pseudomonas aeruginosa etc and could inactivate oxyimino- β -lactams like third-generation cephalosporins and aztreonam, due to their wider substrates for hydrolysis than penicillinase like TEM-1.TEM-2 and SHV-1,were called.Since plasmid mediated SHV-2 type of ESBLs was first reported in German, many new SHV-subtype have been detected and reached 64 varieties by April, 2005. It was mainly produced by Kpn , Eco and other species of Enterobacter. The spreading type of it was different in many countries and areas. Nosocomial infections caused by ESBLs producing strains increased year by year and have been reported to cause epidemic outbreak in some hospitals. Drug-resistance of those strains was currently the most important problem of hospital-acquired drug-resistance in the world.Thus, understanding the best detection of substrate , drug resistance profile and genotypic distribution of ESBLs producing strains can help us prevent regional spreading of ESBLs and guide the proper clinical therapy,in case of delaying instant therapy and causing too much waste.
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