**15.** *E. coli* **sequence type 131 (ST131)**

Determining the clonal types of UPEC is crucial for understanding the role of clonal spread to emerging antimicrobial resistance, which is important for defining and interrupting transmission pathways. Multidrug-resistant *E. coli* sequence type 131 (ST131) has emerged over the past decade as a globally disseminated cause of extraintestinal infections in humans and animals [145–147]. The recent emergence of this clone has coincided with an increase in antibiotic resistance among *E. coli* generally, suggesting a contributing role for ST131 in resistance.

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

UTI pathogenesis is multiply determined. Thus, intervention strategies based on VF genes might have to involve multiple targets, which would offer the extra advantage of protection against a wide range of UTI syndromes. This observation, which is in agreement with previous studies, provides evidence that VF repertoire is as, or more, important than phylogenetic

The Pathogenesis of *Escherichia Coli* Urinary Tract Infection

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The prevalence of antibiotic resistance among human urine *E. coli* isolates has risen substantially in recent years, especially to first line agents such as fluoroquinolones and trimethoprimsulphamethoxazole. Furthermore, multidrug-resistant *E. coli* ST131 has shown rapid global dissemination among humans and animals, which has coincided with the general increase in resistance among *E. coli* clinical isolates. A better understanding of the microbiological basis for the emergence of UPEC antibiotic resistance is necessary for guiding efforts aimed at interrupting this process. Further studies on ST131 are clearly needed to explain its impressive

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[2] Leroy S, Chalumeau T, Ulinski T, et al. Impressive renal damage after acute pyelonephritis

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[6] Griebling TL. Urologic diseases in America project: Trends in resource use for urinary

[7] Ikram R, Rebecca Psutka R, Carter A, Priest P. An outbreak of multi-drug resistant *Escherichia coli* urinary tract infection in an elderly population: A case-control study of

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background for predicting pathogenic behavior in UPEC.

Address all correspondence to: tkudinha@yahoo.com

Clinical Microbiology and Infection. 1999;**6**:328-333

in a child. Pediatric Nephrology. 2010;**25**:1365-1368

Charles Sturt University, Orange, NSW, Australia

Infectious Diseases. 2009;**1**:57-63

**Author details**

Timothy Kudinha

**References**

emergence so that control measures can be devised and implemented.

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 cephalosporin susceptible [148, 149].

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 parts worldwide [141, 152].

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

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 encoded on plasmids carried by the ST131 pandemic clonal group.
