Pap, papG and prsG DNA sequences in Escherichia coli from the fecal flora and the urinary tract

Johanson, Ingmarie; Plos, K.; Marklund, Britt-Inger; Svanborg, Catharina

doi:10.1006/mpat.1993.1062

Cited by 104 publications

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“…Also, of interest in regards to the pap operon among these APEC was that the allele of papG that occurred commonly among APEC was papG allele II, which characterizes the human ExPEC strains causing pyelonephritis [19,20,32]. Similarly, Vandemaele and coworkers [43] reported that papG allele II was the predominant papG allelic variant occurring among the APEC they studied.…”

Section: Discussionmentioning

confidence: 99%

Characterizing the APEC pathotype

et al. 2005

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-The purpose of this study was to compare avian pathogenic Escherichia coli (APEC) isolates to fecal isolates of apparently healthy poultry (avian fecal E. coli or AFEC) by their possession of various traits in order to ascertain whether APEC and AFEC are distinct and if the APEC strains constitute a distinct pathotype. Four hundred and fifty-one APEC and one hundred and four AFEC isolates were examined for possession of traits associated with the virulence of human extraintestinal pathogenic E. coli (ExPEC) as well as APEC. Several of the genes occurred in the majority of APEC and only infrequently in AFEC, including cvaC, iroN, iss, iutA, sitA, tsh, fyuA, irp2, and ompT. Of these genes, several have been found on large plasmids in APEC. Other genes occurred in significantly more APEC than AFEC but did not occur in the majority of APEC. Isolates were also evaluated by serogroup, lactose utilization, and hemolytic reaction. Twenty-nine and a half percent of the APEC and forty-two and three tenths percent of the AFEC were not serogrouped because they were not typeable with standard antisera, typed to multiple serogroups, were rough, autoagglutinated, or were not done. Around 65% of the typeable APEC (205 isolates) and AFEC (41 isolates) were classified into shared serogroups, and about a third of both fell into APEC-(113 isolates) or AFEC-(19 isolates) unique serogroups. Most were able to use lactose. No isolate was hemolytic. Overall, the majority of the APEC isolates surveyed shared a common set of putative virulence genes, many of which have been localized to an APEC plasmid known as pTJ100. This common set of genes may prove useful in defining an APEC pathotype. avian pathogenic Escherichia coli (APEC) / pathotype / virulence plasmid / ExPEC / pTJ100

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Section: Discussionmentioning

confidence: 99%

Characterizing the APEC pathotype

et al. 2005

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“…PapG adhesins at the tip of P-fimbriae mediate specific binding to glycolipid receptors on the uroepithelia and renal tissue; three molecular variants of PapG have been identified (9,10). PapGII (11,12) and PapC (5,13) are suggested to be associated with upper UTI (PN), whereas PapGIII predominates in lower UTI (Cys) (14). In addition to adhesins, other virulence factors (i.e., aerobactin, hemolysin, and capsular polysaccharide) may be associated with the clinical manifestations of PN (12,13,15).…”

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The Role of Host Factors and Bacterial Virulence Genes in the Development of Pyelonephritis Caused by Escherichia coli in Renal Transplant Recipients

Siliano

Rocha

Medina-Pestana

et al. 2010

Clinical Journal of the American Society of Nephrology

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Background and objectives: The aim of this study was to determine the role of host factors and bacterial virulence genes in the development of pyelonephritis caused by Escherichia coli in renal transplant (Tx) recipients.Design, setting, participants, & measurements: A total of 328 E. coli isolates from cases of cystitis (Cys; n ‫؍‬ 239) or pyelonephritis (PN; n ‫؍‬ 89), with 169 from renal Tx recipients, were subjected to molecular analyses to identify P-fimbria subunits (PapC, PapG II, and PapGIII), G-and M-fimbriae, and aerobactin. The presence of antibiotic resistance was also determined. Parameters such as gender, age, immunosuppression regimens, causes of ESRD, kidney donor, intraoperative anastomosis, use of double J stent, trimethoprim/sulfamethoxazole (TMP/SMZ) prophylaxis, and time after Tx were evaluated.Results: A multivariate analysis showed a significant association between PN and renal Tx. In renal Tx recipients, the risk of occurrence of PN was significantly higher among males and for those no longer receiving TMP/SMZ prophylaxis. E. coli strains isolated from PN presented a lower prevalence of papGIII and lower rates of resistance to pipemidic acid. Although papGII was more prevalent in PN than in Cys, it was not independently associated with PN.Conclusions: These findings suggested that renal Tx increases the risk for PN, and the male sex represented a host factor independently associated with risk, whereas the prophylaxis with TMP/SMZ was protective. The lack of papGIII and low resistance to first-generation quinolones were bacterial-independent risk factors for PN in Tx.

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“…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).…”

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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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Pap, papG and prsG DNA sequences in Escherichia coli from the fecal flora and the urinary tract

Cited by 104 publications

References 0 publications

Characterizing the APEC pathotype

Characterizing the APEC pathotype

The Role of Host Factors and Bacterial Virulence Genes in the Development of Pyelonephritis Caused by Escherichia coli in Renal Transplant Recipients

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

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