Pandemic lineages of extraintestinal pathogenic Escherichia coli

Abstract

Pathogenic Escherichia coli strains cause a wide variety of intestinal and extraintestinal infections. The widespread geographical clonal dissemination of intestinal pathogenic E. coli strains, such as E. coli O157:H7, is well recognized, and its spread is most often attributed to contaminated food products. On the other hand, the clonal dissemination of extraintestinal pathogenic E. coli (ExPEC) strains is also recognized, but the mechanism of their spread is not well explained. Here, I describe major pandemic clonal lineages of ExPEC based on multilocus sequence typing (MLST), and discuss possible reasons for their global dissemination. These lineages include sequence type (ST)131, ST393, ST69, ST95, and ST73, which are all associated with both community-onset and healthcare-associated infections, in particular urinary tract infections and bloodstream infections. As with many other types of drug-resistant Gram-negative and Gram-positive bacterial infections, drug-resistant ExPEC infections are recognized to be caused by a limited set of clonal lineages. However, reported observations on these major pandemic lineages suggest that the resistance phenotype is not necessarily the determinant of their clonal dissemination. Both epidemiological factors and their intrinsic biological 'fitness' are likely to contribute. An important public health and clinical concern is that pandemicity itself may be a determinant of progressive drug resistance acquisition by clonal lineages. New research is urgently needed to better understand the epidemiological and biological causes of ExPEC pandemicity.

The Role of Epidemic Resistance Plasmids and International High-Risk Clones in the Spread of Multidrug-Resistant Enterobacteriaceae

“…The exact role of these virulence genes remains to be explained; however, it is possible that a combination of factors contributes to the fitness of ST131 rather than being directly involved in the pathogenesis of infection (79). In vivo studies suggest that fluoroquinolone-resistant E. coli isolates undergo compensatory mutations and become as fit as fluoroquinolone-susceptible isolates (46). This brings up some intriguing issues.…”

“…The term clone has also become useful in molecular epidemiology, particularly in the study of possible relationships between isolates from different geographical areas. It has become well recognized that not all isolates of pathogenic species are necessarily equal and that in a typical pathogenic species, a small number of clones, clusters, or lineages are greatly overrepresented among those isolates recovered from particular types of infection (46).…”

“…High-risk clones most likely possess some types of biological factors that lead to increased "fitness," providing these strains with a Darwinian edge over other isolates of the same species (46). Such advantages will provide them with the abilities to outcontest other bacteria and become the principal part of the bacterial populace in that area.…”

Cutting to the Core of the Issue: Emerging Strategies To Reduce Prostate Biopsy-Related Infections

“…Sensitivities reported for the detection of resistance to fluoroquinolones (75%) and trimethoprim-sulfamethoxazole (74%) are not adequate for clinical use, but this study may serve as a starting point for the development of rapid molecular testing for this application (33). ST131 has disseminated globally and is responsible for much of the increase in antimicrobial-resistant extraintestinal E. coli infections (34). Fluoroquinolone resistance in E. coli, including ST131, is most commonly mediated by mutations in the quinolone resistance-determining region (QRDR) of genes encoding DNA gyrase and topoisomerase IV, gyrA and parC.…”

“…The molecular testing presented, and this approach in general, suffers from several limitations when utilized as an indirect test of fluoroquinolone resistance. This method would fail to detect organisms other than E. coli or those belonging to a different clonal group than the most common, which may be particularly important in geographic regions in which different fluoroquinolone-resistant clones are found (34). Additionally, resistance mediated by the less common mechanisms described, and not associated with a particular clonal group, would not be detected.…”