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Urinary system infections (USI) are mostly caused by Escherichia coli (E.coli) and Klebsiella pneumoniae (K. pneumoniae), which belonging to the family Enterobacteriaceae (1). In the treatment of USI, antibiotic resistance is a challenging problem. In many USI, the treatment fails due to increased bacterial resistance against antibiotics. Moreover, this resistance may also be increased by the antibiotics used in the treatment (2,3). Production of β-Lactamase enzymes is an important mechanism of resistance in Gramnegative bacteria. Many bacterial species such as Klebsiella pneumoniae, Escherichia coli, Proteus mirabilis, and Salmonella carry genes that encode ESBL enzymes (4). β-Lactamase enzymes deactivate the β-Lactam antibiotics by destroying the amide of the β-Lactam ring of the antibiotics. Moreover, these enzymes are synthesized by bacteria via chromosomes, plasmids, or mobile genetic agents known as transposons. Therefore, these enzymes are called extended-spectrum β-Lactamase (ESBL) enzymes (5). ESBL-mediated resistance exhibits resistance to the antibiotics used in the treatment and may lead to serious treatment failure results and high rates of resistance to ESBL-producing bacteria, especially fluoroquinolones, have been reported. However, carbapenems are highly active in the treatment of these infections (6). Identification of ESBL-producing E. coli and K. pneumoniae strains and the knowledge of their rates are of prime importance for the selection of an appropriate antibiotics to the treatment of infectious diseases. ABSTRACT

The Urinary System Infections caused by Extended-Spectrum-β-Lactamase-producing Escherichia coli and Klebsiella pneumoniae Strains