dMaternal-fetal Escherichia coli infections, such as neonatal bacteremia and meningitis, are important causes of morbidity and mortality. From 2006 to 2010, we studied newborns and their mothers who were colonized with E. coli in a French hospital in order to document (i) the epidemiology and genetic characteristics of extended-spectrum-beta-lactamase (ESBL)-producing E. coli strains, (ii) the prevalence of associated virulence genes, (iii) the prevalence of clone sequence type 131 (ST131), and (iv) the genetic relationship among ESBL-producing strains. Among the 2,755 E. coli cultures recovered from vaginal or neonatal samples, 68 were ESBL producers (2.46%). We found a wide diversity of ESBL genes, with the majority being bla CTX-M-14 , bla CTX-M-1 , and bla CTX-M-15 , distributed among the 4 main phylogenetic groups. Genes encoding virulence factors were found in 90.7% of the isolates, with >2 virulence genes present in 76% of cases. The prevalence of ST131 among ESBL-producing E. coli isolates was 9.4% (6/64). Five of these 6 ST131 isolates possessed bla CTX-M-15 enzymes (and also were resistant to quinolones), and one possessed bla CTX-M-2 enzymes. Two possessed virulence genes, suggesting the presence of pathogenicity island II J96 (PAI II J96 )-like domains. Pulsed-field gel electrophoresis (PFGE) revealed a high level of genomic diversity overall, except for 3 closely related isolates belonging to clonal group ST131. Repetitive PCR showed that the six ST131 isolates were closely related to ST131 control strains (>95% similarity). This study shows a high prevalence of ESBL-producing E. coli strains and clonal group ST131 in the French maternal-fetal population. These results suggest a widespread distribution of ESBL enzymes in the community and highlight the early transmission between mothers and neonates. These findings are worrisome, especially for this particularly vulnerable population.
In the past decade, there has been an alarming increase in antibiotic-resistant Enterobacteriaceae producing extended-spectrum beta-lactamases (ESBLs), due at least in part to the overuse of broad-spectrum cephalosporins.The majority of ESBLs identified in clinical isolates during the 1980s to 1990 were of the SHV or TEM type (1). However, since the mid-2000s, CTX-M ESBLs, originating from environmental Kluyvera spp., have gained prominence and are considered pandemic enzymes. CTX-M has been identified in several members of the Enterobacteriaceae family, and especially in Escherichia coli, which has replaced Klebsiella spp. as the principal ESBL-producing member of the Enterobacteriaceae (2-4).ESBL enzymes are important causes of cephalosporin treatment failure. E. coli strains carrying these enzymes were initially responsible mainly for nosocomial infections, but they have now disseminated into the community. One of the best examples of this trend is the global spread of E. coli clone sequence type 131 (ST131), expressing CTX-M enzymes (5). Maternal-fetal E. coli infections, such as neonatal bacteremia and meningitis,...