Objectives To investigate the presumed acquisition of ampicillin resistance by an Escherichia coli strain residing in the gut of an infant.

The ecological impact of antibiotic resistance in the absence of selective pressure has been poorly studied. We assessed the carriage of tetracycline resistance genes, persistence in the microbiota, fecal population counts and virulence factor genes in 309 commensal, intestinal Escherichia coli strains obtained from 128 Swedish infants followed during the first year of life with regular quantitative fecal cultures. No infant was given tetracycline, but 25% received other antibiotics. Tetracycline resistance was identified in 12% of strains, all of which carried either tet (A) (49%) or tet (B) (51%) genes. Resistance to other antibiotics occurred in 50% of tet (A)-positive strains, 42% of tet (B)-positive strains and 13% of tetracycline-sensitive strains. However, colonization with tetracycline-resistant strains was unrelated to treatment with antibiotics. Strains that were tet (B)- or tet (A)-positive carried the genes for P fimbriae and aerobactin, respectively, more often than susceptible strains. Tetracycline-resistant and -susceptible strains were equally likely to persist among the intestinal microbiota for ≥3 weeks and had similar population numbers. However, when a resistant strain and a susceptible strain colonized a child simultaneously, the resistant variety showed lower counts ( P = 0.03). In cases of long-term colonization by initially tetracycline-resistant E. coli strains, loss of tet genes occurred in 3 of 13 cases with variable effects on population counts. The results indicate that there is limited pressure against the carriage of tet genes in the infantile gut microbiota even in the absence of antibiotics. Resistant strains may possess colonization factors that balance the cost of producing resistance elements.

The global emergence of extended-spectrum beta-lactamase-producing Escherichia coli (ESBL-E. coli), mainly causing urinary tract infections (UTI), is of great concern. Almost one third of patients with UTI, develop recurrent UTI (RUTI). We followed 297 patients for one year after their first episode of UTI due to ESBL-E. coli. Our aim was to evaluate the impact of the globally dominant sequence type (ST)131 clone and its clades, on the risk of subsequent recurrences with ESBL-E. coli. Isolates from patients developing RUTI (68/297) were compared with those from patients with sporadic UTI (SUTI, 229/297). No association was found between RUTI and the two most prevalent phylogroups B2 and D, bla_CTX-M genes, or resistance profile. Half of the patients with RUTI were infected with ST131 isolates. Clade C2 were in dominance (50/119) among ST131 isolates. They were more common in patients with RUTI than SUTI (28% vs 13%) and multivariate analysis showed an increased odds-ratio (OR = 2.21, p = 0.033) for recurrences in patients infected with these isolates as compared to non-ST131 isolates. Detecting specific biomarkers, as ST131 clade C2, in ESBL-E. coli UTI isolates may aid in prediction of RUTI and improve diagnostics and care of patients with a risk of ESBL-E. coli recurrences.

To compare the colonization dynamics of ampicillin-resistant and ampicillin-susceptible Escherichia coli strains in the infantile intestinal microbiota. We followed 128 infants over the first year of life with regular quantitative faecal cultures and recordings of antibiotic treatment. E. coli strains were quantified, and their resistance pattern and carriage of β-lactamase genes (TEM, SHV and OXA), phylogenetic group (A, B1, B2 or D), virulence gene profile (fimA, papC, sfaD/E, kfiC neuB, hlyA and iutA) and time of persistence in the microbiota were determined. Twelve percent (n = 32) of the E. coli strains were resistant to ampicillin, as they carried the bla_TEM (84%) or bla_SHV genes. Ampicillin-resistant strains belonged mostly to phylogenetic group D and carried pap genes (P = 0.023) significantly more often than ampicillin-susceptible strains due to a strong association between carriage of pap and bla_SHV. In 31 of 32 cases, colonization by ampicillin-resistant strains occurred in infants not previously treated with β-lactam antibiotics. Ampicillin-resistant strains were equally capable as susceptible ones of persisting in the intestinal microbiota and did not have lower faecal population counts. Genes encoding β-lactamases were in most cases retained during the entire colonization period. The results suggest that ampicillin-resistant E. coli strains are not hampered in their colonizing capacity, and β-lactamase genes, therefore, may only slowly be eliminated from the commensal E. coli strain pool.

P fimbriae, enabling adherence to colonic and urinary epithelium, and aerobactin, an iron sequestering system, are both colonization factors in the human colon and virulence factors for urinary tract infection. The colonic microbiota is suggested to be a site suitable for the transfer of antibiotic resistance genes. We investigated whether phenotypic resistance to antibiotics in commensal and uropathogenic Escherichia coli from infants and young children is associated with carriage of virulence genes and to phylogenetic group origin and, in the case of fecal strains, to persistence in the gut and fecal population levels. The commensal strains (n = 272) were derived from a birth cohort study, while the urinary isolates (n = 205) were derived from outpatient clinics. Each strain was assessed for phenotypic antibiotic resistance and for carriage of virulence genes (fimA, papC, sfaD/E, hlyA, iutA, kfiC, and neuB), phylogenetic group (A, B1, B2, or D), and markers of particular virulent clones (CGA-D-ST69, O15:H1-D-ST393, and O25b:H4-B2-ST131). Resistance to ampicillin, tetracycline, and trimethoprim was most prevalent. Multivariate analysis showed that resistance to any antibiotic was significantly associated with carriage of genes encoding P fimbriae (papC) and aerobactin (iutA), and a phylogenetic group D origin. Neither fecal population numbers nor the capacity for long-term persistence in the gut were related to antibiotic resistance among fecal strains. Our study confirms the importance of phylogenetic group D origin for antibiotic resistance in E. coli and identifies the virulence genes papC and iutA as determinants of antibiotic resistance. The reason for the latter association is currently unclear.

The bacterial features associated with recurrent urinary tract infections (RUTIs) due to extended-spectrum beta-lactamase-producing Escherichia coli (ESBL-E. coli) are not well-understood. We investigated phylogenetic groups and ST131 subclones to assess strain homology of ESBL-E. coli isolates in patients with RUTIs from the in- and out-patient setting in western Sweden. Almost all (319/356) isolates from 123 patients with 2-7 episodes (median 2) of ESBL-E. coli UTI within 1 year were examined for seven E. coli phylogroups, the ST131-O25b clone, and its subclone fimH30Rx. Antibiotic resistance and ESBL-genes were determined for the index isolates. A subset of isolates was typed using pulsed-field gel electrophoresis. The same phylogroup and ST131 subclones were seen for all recurrences in 119/123 patients and PFGE confirmed strain homology in recurrences for 43/44 patients tested. Phylogroup B2 dominated (56%), followed by D (19%) and F (10%). ST131-O25b and fimH30Rx isolates were detected in 44% and 30%, respectively. CTX-M group 1 (71%) predominated. Elderly patients were in majority. There were no associations between patient demographics or time to recurrence and bacterial characteristics. The fimH30Rx subclone was associated with a higher number of recurrences (p = 0.015) as compared to the remaining B2 isolates. In ESBL-E. coli RUTI, most recurrences were caused by the initial infecting strain. The high frequency of the multidrug-resistant fimH30Rx subclone and its association with multiple recurrences warrants further attention and early detection of this subclone in patients at risk of developing RUTI with ESBL-producing E. coli.