**Author details**

In contrast to traditional antimicrobial resistant *E. coli*, which mostly derive from low virulence phylogenetic groups A and B1, ST131 derives exclusively from phylogenetic group B2, which is traditionally known to be enriched for VF genes. This, plus limited experimental evidence of virulence and several case reports of unusually severe or fatal extraintestinal infections due to ST131, suggests that the emergence of ST131 may be due to a high virulence potential (in addition to antibiotic resistance) compared with other *E. coli* types. However, despite this, some studies have reported absence of traits commonly associated with B2 phylogeny, particularly

Most ST131 clinical isolates are FQ resistant, and many are also co-resistant to aminoglycosides and/or trimethoprim-sulfamethoxazole (TMP-SMZ). A minority produces extended-spectrum beta-lactamases (ESBLs) that confer resistance to extended-spectrum cephalosporins. *E. coli* clonal group ST131 may be associated with other beta-lactamases but some isolates are cephalo-

Despite limited epidemiological evidence of increased virulence of ST131, a recent study revealed that ST131 exhibits a marked prevalence gradient across source groups, from pyelonephritis to cystitis isolates, and finally to fecal isolates [126]. This is consistent with increased urovirulence, and provides epidemiological evidence of increased virulence for ST131, which has been presumed but without evidence from experimental animal models [8, 150]. The antibiotic resistance advantage, in combination with the possible presence of enhanced virulence, could explain the recent worldwide emergence of ST131. The increasing prevalence of ESBLproducing *E. coli* has been associated with the emergence of CTX-M-ST131 pandemic clonal group [151]. Available evidence supports that ST131 is an important contributor to the spread of ESBLs among reproductive-age women in some regions, albeit limited research in many

Four VF genes (*iutA, ompT, usp*, and *traT*) are associated with ST131 isolates, and so could represent potential targets for vaccines or other interventions, particularly if a functional role in virulence or dissemination can be demonstrated for them. Most of the ST131 isolates (85%)

Resistance of ST131 to extended-spectrum cephalosporins is often due to production of ESBLs. The initial descriptions of ST131 emphasized its association with CTX-M-15, but subsequent studies have shown that it is more commonly ESBL-negative but FQ-resistant [154–156]. Previous studies in Australia and Japan showed that ST131-O25b, ST131-O16, and group D-ST405 clonal groups contribute to the spread of ESBL-producing *E. coli* [151, 152]. The dominant ESBL, in *E. coli*, globally and in Australia [157] is CTX-M-15, which is frequently

A wide range of UPEC VFs have been established epidemiologically or experimentally (*in vivo*) as being important in UTI pathogenesis. No single VF profile has been proven to be important in causing any particular UTI syndrome. Indeed, studies have suggested that

are of the O25b variant, and the remainder are type O16 [153, 154].

encoded on plasmids carried by the ST131 pandemic clonal group.

adhesins (e.g., P, S, and FIC fimbriae) and toxins (e.g., hemolysin and cnf1).

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

sporin susceptible [148, 149].

parts worldwide [141, 152].

**16. Conclusions**

Timothy Kudinha

Address all correspondence to: tkudinha@yahoo.com

Charles Sturt University, Orange, NSW, Australia
