**Author details**

The prevalence of *hly* gene in *cdt*-type III, IV, and V was more than other isolates. These results demonstrate that, possibly, there could be a relationship between the existence of *hly* gene and the type of *cdt* gene in clinical *E. coli* isolates. *fliC* and *fim* are two chromosomally located genes that can be defined as the genomic background of *E. coli* strains. The *fliC* gene encodes the flagel‐ lin subunit; type 1 fimbriae are also encoded by the chromosomally located *fim* gene cluster. The presence of *fim* DNA sequences is common among *E. coli* strains. In fact, the majority of clinical isolates, both virulent and non-virulent, could be induced to express type 1 fimbriae [19].

328 *Escherichia coli* Escherichia coli - Recent Advances on Physiology, Pathogenesis and Biotechnological Applications - Recent Advances on Physiology, Pathogenesis and Biotechnological Applications

Among pathogenic *E. coli*, the existence of a large virulent plasmid (pO157) has also been observed. The *etpD*, *katP*, and *espP* genes are located on this plasmid. The pO157 plasmid is mainly associated with EHEC and ETEC strains. There is a relation between the occurrence of *stx* genes and these virulent plasmid-associated genes. Moreover, PCR analysis revealed a close relationship between the occurrence of plasmid-born *katP* gene and *stx* gene in patho‐ genic *E. coli.* Most of the *katP*+ strains belong to Shiga toxin-producing *E. coli.* The *katP* gene is mostly present in CDT-I- and CDT-II-producing strains. EspP, which possesses human coagulation factor V and pepsin A proteolytic activity, is a significant marker of virulence in Shiga toxin-producing strains. In CDT-III-producing isolates, high frequency of *espP gene* is considerable. Alpha-hemolysin is frequently associated with human uropathogenic *E. coli* (UPEC); furthermore, related encoding PAI is also unstable and the operon could be located on either a plasmid or the chromosome. Besides, urinary tract infection (UTI) is caused pre‐ dominantly by type 1fimbriated UPEC and initial binding is mediated by the FimH adhesin

*katP*, and *espP.* These genes plus the *stx* gene are among the EHEC and STEC characteristics, although the *espP* gene is common in EPEC and EHEC. Simultaneous presence of these genes indicates that clinical isolates obtain *hly* operon and relevant PAI. In addition, in evolutionary pathways, isolates improve their pathogenicity by achieving the *cdt* genes. Studies demon‐ strate that virulence genes from CDT-producing strains belong to the heterogeneous group. Strains which are clustered as particular groups have similar characteristics, while possessing their own unique genotype and genomic content. For instance, each distinct *cdt*-type group, by possessing a particular *cdt* gene as genomic backbone, has an approximately similar pat‐

This evidence further confirms that horizontal gene transfer could occur among pathogenic strains. Moreover, findings indicate that CDT-producing strains may have originated from a common ancestor during their evolution by HGT, and they departed from each other [17].

CDT-producer strains did not show particular phylogenomic relation and pattern. Indeed, they might carry the same or similar virulence gene sets, but remarkably possess their own divergent genomic structure. This is probably because of their complex and distinct evolu‐ tionary pathways, indicating independent acquisition of mobile genetic elements that have driven from their evolution [19]. Furthermore, it was shown that there are different types of CDTs that are encoded by prophages, plasmids, and/or pathogenicity islands that result in

strains possess one or more of plasmid pO157 genes, including *etpD*,

strains harbor *fimH*

of the mentioned fimbriae. Investigation showed that most of the *hly*<sup>+</sup>

different types of CDTs through HGT in different origins [7, 17, 19, 22].

gene. In addition, all *hly*<sup>+</sup>

tern based on other virulence genes [19].

Maryam Javadi, Saeid Bouzari and Mana Oloomi\* \*Address all correspondence to: manaoloomi@yahoo.com Molecular Biology Department, Pasteur Institute of Iran, Tehran, Iran
