Phylogenetic, virulence and antibiotic resistance characteristics of commensal strain populations of Escherichia coli from community subjects in the Paris area in 2010 and evolution over 30 years

Abstract

Editor's Choice Phylogenetic, virulence and antibiotic resistance characteristics of commensal strain populations of Escherichia coli from community subjects in the Paris area in 2010 and evolution over 30 years It is important to study commensal populations of Escherichia coli because they appear to be the reservoir of both extra-intestinal pathogenic E. coli and antibiotic resistant strains of E. coli. We studied 279 dominant faecal strains of E. coli from 243 adults living in the community in the Paris area in 2010. The phylogenetic group and subgroup [sequence type complex (STc)] of the isolates and the presence of 20 virulence genes were determined by PCR assays. The O-types and resistance to 18 antibiotics were assessed phenotypically. The B2 group was the most frequently recovered (34.0 %), followed by the A group (28.7 %), and other groups were more rare. The most prevalent B2 subgroups were II (STc73), IV (STc141), IX (STc95) and I (STc131), with 22.1, 21.1, 16.8 and 13.7 %, respectively, of the B2 group strains. Virulence factors (VFs) were more common in B2 group than other strains. One or more resistances were found in 125 strains (44.8 % of the collection) but only six (2.2 % of the collection) were multiresistant; no extended-spectrum beta-lactamase-producing strain was isolated. The C phylogroup and clonal group A strains were the most resistant. No trade-off between virulence and resistance was evidenced. We compared these strains with collections of strains gathered under the same conditions 30 and 10 years ago. There has been a parallel and linked increase in the frequency of B2 group strains (from 9.4 % in 1980, to 22.7 % in 2000 and 34.0 % in 2010) and of VFs. Antibiotic resistance also increased, from 22.6 % of strains resistant to at least one antibiotic in 1980, to 31.8 % in 2000 and 44.8 % in 2010; resistance to streptomycin, however, remained stable. Commensal human E. coli populations have clearly evolved substantially over time, presumably reflecting changes in human practices, and particularly increasing antibiotic use.

Iron Homeostasis Regulates the Genotoxicity of Escherichia coli That Produces Colibactin

“…Moreover, the main reservoir of E. coli is the intestine and, more precisely, the colon. A recent publication confirmed the emergence of the B2 group of E. coli in developed countries (34). Given the existence of a gradient of iron concentration from the lumen to the intestinal epithelial cell, it is conceivable that the fine-tuning of clbA expression allows the production of colibactin when the pathogenic E. coli isolate is located in an appropriate site in the gut.…”

Plasmid-mediated quinolone resistance determinants in quinolone-resistant Escherichia coli isolated from patients with bacteremia in a university hospital in Taiwan, 2001–2015

“…Massot et al showed a parallel and linked increase in the frequency of the B2 group strains (from 9.4% in 1980 to 22.7% in 2000 and 34.0% in 2010) and of virulence factors18. Here, we showed 38.7% of the FQ-resistant bacteremia E. coli isolates belonged to phylogenetic group B2, followed by group B1 (23.4%), group A (22.6%), group D (14.9%), and group F (0.4%) (Table 1).…”

Long‐term evolution of the natural isolate of Escherichia coli 536 in the mouse gut colonized after maternal transmission reveals convergence in the constitutive expression of the lactose operon

“…Furthermore, the more consistent maintenance of E. coli 536 in the WD diet is probably due to its genetic background rather than to de novo adaptation as we failed to see a clear signature of adaptation. The maintenance of a B2 background with WD echoes the spread of the phylogenetic group B2 (to which E. coli 536 belongs), in a commensal situation, in the digestive tract of individuals living in industrialized countries (Tenaillon et al, ) for the past 30 years (Massot et al, ). This model seems therefore consistent with some epidemiological patterns of commensal E. coli in the human gut, suggesting its relevance.…”