The incidence of nosocomial bacteremia caused by gramnegative aerobic bacilli has increased markedly over the past two decades. Klebsiella spp. ranked second only to Escherichia coli as etiological agents of gram-negative sepsis [1]. Klebsiella pneumoniae accounted for a significant proportion of hospital-acquired urinary tract infections, pneumonia, septicemias, and soft tissue infections. Pneumonias caused by K. pneumoniae are difficult to treat and mortality rates can reach up to 50% even after antibiotic therapy, indicating the relative ineffectiveness of current antibiotic therapy for such infections [2]. K. pneumoniae often cause extensive lung destruction [3].

K. pneumoniae is naturally resistant to many common antibiotics. K. pneumoniae has been known to be resistant to penicillin, especially ampicillin and carbenicillin via the action of penicillinase SHV-1. About 30 years ago, a second blactamase, TEM-1 appeared [4]. In the mid 1980s, ESBL K. pneumoniae strains that were resistant to extended spectrum b-lactams and third-generation cephalosporins appeared worldwide [4]. ESBLs are plasmid-mediated, thereby con-