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Extended-spectrum b-lactamases (ESBLs) are enzymes that confer resistance to penicillins, narrowand extended-spectrum cephalosporins, monobactams and related oxyimino-b-lactams (ceftazidime, cefotaxime) and have been shown to be inactive against cephamycins and carbapenems (Bradford, 2001; Bradford et al., 1994; Bush et al., 1995; Pitout and Sanders, 1997). Clavulanate, tazobactam and other blacamase inhibitors are generally effective against ESBLs although some inhibitor resistant variants have been described (Bradford, 2001; Bradford et al., 1994; Bush et al., 1995). Bacteria producing ESBLs are most commonly Klebsiella pneumoniae and Escherichia coli, as well as other members of the genus in Enterobacteriaceae (Jarlier et al., 1998). In Lebanon, a study done at a general hospital in Beirut in 1998 (Araj, 1999) revealed that the prevalence of ESBL-producing E. coli and K. pneumoniae isolates was 3.3% and 6.4%, respectively. At Saint George University Hospital, a 300-bed hospital participating in our study, 2% of 4,299 isolates of E. coli and 20% of 1,248 isolates of K. pneumoniae were found to produce ESBLs between 1997 and 2001 (Daoud and Hakime, 2003). In fact, the percentage of these had been experiencing a constant rise over the 5 years from 7.5% to 24% for Klebsiella pneumoniae and reached 4% for Escherichia coli (Daoud and Hakime, 2003).

Numerous ESBL enzymes have been described, with greater than 100 in the TEM class, over 40 in the SHV family, over 30 in the CTX-M class, and 15 in the OXA family (Bonnet, 2004; Bradford, 2001). These enzymes are coded by plasmids which may also carry …