Distribution of papG alleles among uropathogenic Escherichia coli isolated from different species

Féria, C

doi:10.1016/s0378-1097(01)00310-x

Cited by 20 publications

(13 citation statements)

References 18 publications

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“…Indeed, the bla TEM‐1G gene, present in a canine E. coli strain, has the same framework as a gene encoding an IRT β‐lactamase produced in an E. coli strain of human origin. This is consistent with the recent demonstration of the zoonotic potential of uropathogenic E. coli strains [13,14].…”

Section: Resultssupporting

confidence: 93%

A novel sequence framework (bla_TEM-1G) encoding the parental TEM-1 beta-lactamase

Pomba-Féria¹,

Caniça

2003

FEMS Microbiology Letters

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A novel parental bla TEM gene (bla TEMÀ1G ), encoding a TEM-1 L-lactamase (pI of 5.4) produced by the uropathogenic Escherichia coli strain FMV194 was isolated from a dog. We report PCR^restriction fragment length polymorphism analysis and nucleotide sequencing of this gene. The bla TEMÀ1G sequence was identical to the bla TEMÀ1C gene framework in the coding and promoter (P3) regions, except for a silent G 604 CT mutation in the coding region. Molecular phylogenetic analysis of parental bla TEM genes indicated two distinct groups, one comprising bla TEMÀ1F and bla TEMÀ2 . The other group comprises bla TEMÀ1C which is the probable ancestor of bla TEMÀ1A , bla TEMÀ1D and bla TEMÀ1G . The bla TEMÀ1G gene has the same framework as a gene encoding an inhibitor-resistant TEM L-lactamase produced by an E. coli strain of human origin. Thus, parental bla TEM genes encoding L-lactamases in E. coli strains isolated from different host species, in this case human and canine, may be phylogenetically very close. ß

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Section: Resultssupporting

confidence: 93%

A novel sequence framework (bla_TEM-1G) encoding the parental TEM-1 beta-lactamase

Pomba-Féria¹,

Caniça

2003

FEMS Microbiology Letters

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“…One may speculate that E. coli from a family cat could be transferred to the infant, because E. coli causing urinary tract infection in cats and dogs frequently carry the papG III adhesin type, and these strains arise from the intestinal flora of the animals (16,17). We saw no effect on E. coli gene carriage by dog-ownership.…”

Section: Discussionmentioning

confidence: 59%

“…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 common in cystitis strains from humans (15), dogs (16), and cats (17). Intestinal persistence of E. coli has been linked to the class II variety of the adhesin (10).…”

mentioning

confidence: 99%

Escherichia coli in Infants' Intestinal Microflora: Colonization Rate, Strain Turnover, and Virulence Gene Carriage

et al. 2003

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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...

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“…P pili, encoded on the pap operon, bind through the PapG adhesin to terminal sugars of glycolipids present on the surface of host cells. Host and tissue specificity varies due to the presence of different PapG adhesins recognizing different but related Gala-(1-4)-Gal sugars (Feria et al, 2001). The fim gene cluster encodes type I pili, with FimH being the pilus adhesin.…”

Section: Type I and P Pilimentioning

confidence: 99%

Protein secretion systems and adhesins: The molecular armory of Gram-negative pathogens

Gerlach¹,

Hensel²

2007

International Journal of Medical Microbiology

243

285

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Distribution of papG alleles among uropathogenic Escherichia coli isolated from different species

Cited by 20 publications

References 18 publications

A novel sequence framework (bla_TEM-1G) encoding the parental TEM-1 beta-lactamase

A novel sequence framework (bla_TEM-1G) encoding the parental TEM-1 beta-lactamase

Escherichia coli in Infants' Intestinal Microflora: Colonization Rate, Strain Turnover, and Virulence Gene Carriage

Protein secretion systems and adhesins: The molecular armory of Gram-negative pathogens

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Distribution of papG alleles among uropathogenic Escherichia coli isolated from different species

Cited by 20 publications

References 18 publications

A novel sequence framework (blaTEM-1G) encoding the parental TEM-1 beta-lactamase

A novel sequence framework (blaTEM-1G) encoding the parental TEM-1 beta-lactamase

Escherichia coli in Infants' Intestinal Microflora: Colonization Rate, Strain Turnover, and Virulence Gene Carriage

Protein secretion systems and adhesins: The molecular armory of Gram-negative pathogens

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A novel sequence framework (bla_TEM-1G) encoding the parental TEM-1 beta-lactamase

A novel sequence framework (bla_TEM-1G) encoding the parental TEM-1 beta-lactamase