K. pneumoniae is a facultative anaerobic, Gram negative bacteria of the Enterobacteriaceae family, and a reported opportunistic pathogen that has been implicated in many community- and hospital-acquired infections . This organism can initiate urinary tract infections, wound infections, pneumonia, intra-abdominal infections, nasal mucosa atrophy, and rhinoscleroma. The number of outbreaks involving K. pneumoniae strains with extended spectrum β-lactamase (ESBL) mediated resistance to third-generation cephalosporins has been progressively increasing in many parts of the world .
β-lactamases, the precursors to ESBLs, confer resistance by inactivating β-lactam antibiotics , like penicillins, cephalosporins, carbapenems, and monobactams, by breaking open the four atom β-lactam ring structure. The extended spectrum β-lactamases (ESBLs) are a rapidly developing group of enzymes with the ability to hydrolyze third-generation cephalosporins as well as the monobactams and aztreonams that are known to be active against Klebsiella species. Clavulanic acid is a potent inhibitor of the β-lactamases and is commonly included with β-lactam antibiotics when an ESBL-producing bacterium is suspected. Clavulanic acid is a member of the clavams or oxapenams that inhibits β-lactamase activity by cova-lently binding to the serine that resides in the active site of the enzyme.
ESBL genes originally evolved from the β-lactamase TEM-1, TEM-2, and SHV-1 genes through mutations of the amino acids surrounding the active site β-lactamases.
ESBLs have recently become a significant problem because they are commonly plasmid-encoded, facilitating a high rate of horizontal transfer between different bacterial species . Furthermore, such plasmids typically carry resistance genes to other drugs such as the aminoglycosides, thus narrowing treatment options.
As an illustration, administration of cephalosporins has recently been linked to increasing treatment failure rates, and isolated strains have been found to possess higher minimal inhibitory concentration (MIC) rates for ceftriaxone, cefotaxime and, to a lesser extent, ceftazidime. However, this resistance diminishes in the presence of β-lactamase inhibitors, such as clavulanic acid . This type is considered class-A ESBL resistance, where the TEM, SHV and CTX-M type ESBL enzymes are able to hydrolyze .
Previous molecular characterization studies on TEM, SHV, and CTX-m genes and their derivatives, e.g. bla TEM-1 and bla SHV-12, have shown that they are epidemiologically related, and are both plasmid-borne . PFGE have also been widely employed to investigate the epidemiological and genotypic relatedness of ESBL-producing bacteria  and to track evolving strains implicated in various geographic regions . Recent studies in the Middle East have revealed a high prevalence of ESBL-producing K. pneumoniae isolates in Israel , and extensive spread of those carrying CTX-m-15 was reported in Lebanon, Kuwait, and Egypt [8–10]. In Saudi Arabia, CTX-M-15 producing K. pneumoniae was responsible for a neonatal intensive care unit outbreak .
Our goal was to characterize and determine the prevalence of genetic elements of ESBL-producing K. pneumoniae collected between 2000 and 2003 in Egypt. Isolates in this study including those from both community-acquired and nosocomial infections, were genotyped and their DNA fingerprints were compared.