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ABSTRACTThe mannose-specific adhesin of type 1 fimbriae is the most common adhesin in Escherichia coli. One receptor for this adhesin is the carbohydrate chains of secretory immunoglobulin A (S-IgA), and intestinal E. colifrom IgA-deficient individuals has a reduced capacity to adhere to mannose-containing receptors. Here, we investigated the expression of the mannose-specific adhesin and its capacity to switch to the fimbriated phenotype in colonic resident and transient E. colistrains isolated from control (n= 16) and IgA-deficient (n= 17) persons. Resident E. colistrains from IgA-deficient individuals displayed weaker mannose-specific adherence to colonic cells than resident strains from control individuals (21 versus 44 bacteria/cell, P= 0.0009) due to three mechanisms: a lower carriage rate of the fimHgene (90% versus 97%, not significant), more frequent failure to switch on the fimgenes (30% versus 6%, P= 0.02), and the reduced adhesive potential of fimH+isolates capable of phase switch (26 versus 46 bacteria/cell, P= 0.02). On the other hand, resident strains from IgA-deficient individuals displayed stronger mannose-resistant adherence than resident strains from control individuals (P= 0.04) and transient strains from IgA-deficient individuals (P= 0.01). The presence of S-IgA appears to favor the establishment of E. coliclones which readily express mannose-specific adhesins in the bowel microbiota.

ABSTRACTThe 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 colistrains 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. colistrains, loss of tetgenes occurred in 3 of 13 cases with variable effects on population counts. The results indicate that there is limited pressure against the carriage of tetgenes 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.

Colonization by Escherichia. coliin infants might have decreased in the last decades, owing to changes in hospital routines and family lifestyle. In this study, the E. coliflora was characterized in 70 healthy Swedish infants followed for the first year of life. E. coliwas isolated from rectal swabs obtained at 3 d of age and quantified in fecal samples collected at 1, 2, 4, and 8 wk of age and at 6 and 12 mo of age. Strains were typed using random amplified polymorphic DNA, and their virulence factor genes were identified by multiplex PCR. Colonization by E. colioccurred late only 61 of the infants were positive by 2 mo of age. The turnover of individual strains in the microflora was slow 1.5 strains per infant during 6 mo, 2.1 during 1 y. Environmental factors, such as siblings, pets, or feeding mode, did not influence colonization kinetics or strain turnover rate. Genes encoding type 1 fimbriae, P fimbriae, and hemolysin were significantly more common in E. colistrains persisting for at least 3 wk in the microflora than in transient strains. The Pfimbrial class III adhesin gene was more common in E. colifrom children who had a cat in their homes than in E. colifrom children without pets p0.01 this adhesin type is common in E. colifrom cats. The late colonization and low E. colistrain turnover rate suggest limited exposure of Swedish infants to E. coli.Our results confirm that P fimbriae and other virulence factors facilitate persistence of E. coliin the human colonic microflora.

Staphylococcus aureushas been isolated at an increasing rate from infants’ stools during the last decades, but it is not known whether this species can colonize and persist in the intestinal microflora. To investigate this, 49 Swedish infants were followed prospectively from birth until 12 months of age. S. aureuswas identified in a rectal swab obtained 3 d after delivery and in quantitative cultures of fecal samples collected at 1, 2, 4, and 8 weeks and at 6 and 12 months of age. A random amplified polymorphic DNA (RAPD) method was developed to distinguish individual S. aureusstrains from one another and the strains were tested for production of enterotoxins A-D and TSST-1. By 3 days of age, 16 of infants had S. aureusin their intestines, which increased to 73 by 2-6 months, whereafter it decreased slightly to 53. At the same time S. aureuspopulation counts in colonized infants declined from an average 106.8CFU/g feces during the first months of life to 104.0CFU/g feces by 12 months. Colonized infants usually harbored one or two S. aureusstrains in their microflora for long periods of time. Few strains were transient passengers and the median time of persistence of S. aureusstrains in the microflora was several months. Of the 75 S. aureusstrains identified, 43 produced one or more toxins 13 SEA, 7 SEB, 23 SEC, 4 SED, and 11 TSST-1. Altogether, 47 of the investigated infants were colonized by a toxin-producing S. aureusduring their first year of life. Despite this they were apparently healthy and did not have more gastrointestinal problems than noncolonized infants. This report is the first to show that S. aureusmay be a resident member of the normal intestinal microflora in infancy.