Escherichia coli strains segregate into 4 phylogenetic groups, designated "A," "B1," "B2," and "D." Pathogenic strains belong to group B2 and, to a lesser extent, group D, which more frequently carry virulence-factor genes than do group A strains and group B1 strains. This study investigated whether the capacity of E. coli to persist in the human intestine is related to its phylogenetic type. Resident (n=58) and transient (n=19) commensal E. coli strains isolated during a longitudinal study of 70 Swedish infants and previously tested for virulence-factor-gene carriage were tested for phylogenetic type. Of the strains resident in the intestinal microflora, 60% belonged to group B2, compared with only 21% of the transient strains (P=.004). In logistic regression, group B2 type predicted persistence in the intestinal microflora, independent of carriage of all investigated virulence-factor genes, including genes for P fimbriae (P=.03). Thus, group B2 strains appear to possess yet unidentified traits that enhance their survival in the human intestine.

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Colonization by Escherichia. coli in infants might have decreased in the last decades, owing to changes in hospital routines and family lifestyle. In this study, the E. coli flora was characterized in 70 healthy Swedish infants followed for the first year of life. E. coli was 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. coli occurred 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. coli strains persisting for at least 3 wk in the microflora than in transient strains. The P-fimbrial class III adhesin gene was more common in E. coli from children who had a cat in their homes than in E. coli from children without pets (p ϭ 0.01); this adhesin type is common in E. coli from cats. The late colonization and low E. coli strain 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. coli in the human colonic microflora. Escherichia coli is one of the first bacterial species to colonize the infant's intestines. In the 1970s, E. coli usually appeared in the baby's feces a few days after birth (1, 2), as a sign of its establishment in the intestinal microflora (3, 4). E. coli colonizing the newborn infant may originate in the maternal fecal flora (5), but E. coli strains are also commonly spread at maternity wards via the nursing staff, especially during periods of high bed-occupancy and staff workload (6). We have recently reported that Staphylococcus aureus has become a major colonizer of the infant gut (7), which may be a sign of reduced competition from other microbes. E. coli and other fecal bacteria might be less easily spread today, because of increased hygiene in hospitals and families.Some E. coli strains persist in the intestinal microflora of an individual for months or years (resident strains), whereas others (transient strains) disappear within a few weeks (8). Resident E. coli strains display certain characteristics that enable them to persist in the intestinal microflora, e.g. the expression of P fimbriae and capacity to adhere to colonic epithelial cells (9 -12). P fimbriae are composed of a fimbrial rod with a tip adhesin that exists in three varieties, termed papG classes I, II, and III. These recognize the Gal␣134Gal␤ disaccharide, with slight differences in binding specificity (13). The class II variety of the papG adhesin is common among E. coli causing pyelonephritis (14), whereas the class III variety is comm...

Staphylococcus aureus has 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. aureus was 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. aureus strains 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. aureus in their intestines, which increased to 73% by 2-6 months, whereafter it decreased slightly to 53%. At the same time S. aureus population counts in colonized infants declined from an average 10 6.8 CFU/g feces during the first months of life to 10 4.0 CFU/g feces by 12 months. Colonized infants usually harbored one or two S. aureus strains in their microflora for long periods of time. Few strains were transient passengers and the median time of persistence of S. aureus strains in the microflora was several months. Of the 75 S. aureus strains 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. aureus during 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. aureus may be a resident member of the normal intestinal microflora in infancy. Abbreviations CFU, colony-forming units TSST-1, toxic shock syndrome toxin-1 RAPD, random amplified polymorphic DNA Bacteria start to colonize the skin, respiratory tract, and intestines as soon as the newborn has left the sterile womb. With time, a complex ecosystem develops known as the normal microflora (1). Staphylococcus aureus colonizes the anterior nares of more than 50% of young infants (2-5). During the last decades, S. aureus has also been isolated at an increasing rate from fecal samples of infants in Western societies. Thus, only 1 out of 13 infants had S. aureus in their stools in a study performed in England in the 1980s (6), but 30% in a Swedish study published 1985 (7) and 53% in Sweden in the late 1990s (8). It is not known whether staphylococci persist and replicate in the intestines or if S. aureus in the stools represent bacteria transiently passing the intestines after having been swallowed. If infants are colonized by S. aureus in their intestines, it may have medical consequences. S. aureus strains can produce a range of different exotoxins, among them the enterotoxins, which cause vomiting with or without diarrhea and are responsible for staphylococcal food poisoning (9). The enterotoxins, together with toxic shock syndrome toxin-1, also function as "superantigens." By binding to both...

Resident and transient Escherichia coli strains from the colonic microflora of 13 Swedish schoolgirls were analysed for carriage of genes encoding a range of adhesins (P, type 1 and S fimbriae, Dr haemagglutinin and three varieties of the P fimbrial papG adhesin) and other virulence traits (K1 and K5 capsule, haemolysin and aerobactin) using multiplex PCR. Forty-four percent of the resident clones carried genes for P fimbriae, K1 or K5 capsule, and aerobactin, compared with only 3% of transient clones (P<0·0001). The P-fimbriated clones most often had the class II variety of the P-fimbrial adhesin gene papG and this adhesin was significantly associated with persistence of a strain. S fimbriae and type 1 fimbriae were equally common in resident and transient strains. The results indicate that not only P fimbriae, but also, certain capsules and the ability to produce the siderophore aerobactin might contribute to persistence of E. coli in the large intestine.

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.

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Virulence-associated genes in bacteria are often located on chromosomal regions, termed pathogenicity islands (PAIs). Several PAIs are found in Escherichia coli strains that cause extraintestinal infections, but their role in commensal bowel colonization is unknown. Resident strains are enriched in adhesins (P fimbriae and type 1 fimbriae), capsular antigens (K1 and K5), hemolysin, and aerobactin and mostly belong to phylogenetic group B2. Here, we investigated whether six pathogenicity islands and the virulence determinants malX and usp are associated with fitness of E. coli in the infant bowel microbiota. E. coli strains isolated from stools of 130 Swedish infants during the first year of life were examined for their carriage of PAI markers, malX, and usp by PCR. Carriage was related to strain persistence: long-term colonizers (>12 months) carried significantly more of PAI II from strain CFT703 (II CFT703 ), IV 536, and II J96 and malX and usp than intermediate colonizers (1 to 11 months) and transient strains (<3 weeks). The accumulation of PAI markers in each individual strain correlated positively with its time of persistence in the colon. Phylogenetic group B2 accounted for 69% of long-term colonizers, 46% of intermediate colonizers and 14% of transient strains. These results support the hypothesis that some bacterial traits contributing to extraintestinal infections have in fact evolved primarily because they increase the fitness of E. coli in its natural niche, the colon; accordingly, they may be regarded as fitness islands in the gut.Escherichia coli is a normal inhabitant of the large intestine, but certain strains also cause extraintestinal infections when they spread from their primary niche. Such pathogenic E. coli strains express several virulence-associated traits that contribute to the disease process, including adhesins, certain O serotypes and capsular antigens, iron-trapping compounds (such as aerobactin), and cytolytic toxins (such as hemolysin) (17).Pathogenicity-associated islands (PAIs) are particular regions on the bacterial chromosome where virulence genes have accumulated. PAIs, and their associated virulence genes, have spread among bacterial populations by horizontal transfer (15). Several PAIs were previously identified in uropathogenic E. coli strains such as E. coli 536 , E. coli J96, and E. coli CFT073. PAIs I to IV from strain 536 (I 536 to IV 536 ) encode a range of virulence factors, including P fimbriae, P-related fimbriae, ␣-hemolysin, S fimbriae, and the yersiniabactin siderophore system. PAI I J96 and II J96 encode P fimbriae, P-related fimbriae, and ␣-hemolysin; PAI I CFT073 and II CFT073 encode P fimbriae, ␣-hemolysin, and aerobactin (42) ( Table 1). usp is prevalent among strains causing urinary tract infections (24). It enhances infectivity in a mouse ascending urinary tract infection (UTI) model (48), displays homology with S-type pyocin, and may function as a bacteriocin (34). malX codes for a phosphotransferase system enzyme II that recognizes maltose and glucose (37...