Molecular epidemiology of adhesin and hemolysin virulence factors among uropathogenic Escherichia coli

Arthur, Michel; Johnson, Carrie; Rubin, Robert H.; Arbeit, Robert D.; Campanelli, Craig; Kim, Cheung; Steinbach, Suzanne; Agarwal, Manju; Wilkinson, Ray; Goldstein, Richard

doi:10.1128/iai.57.2.303-313.1989

Cited by 160 publications

(89 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The papG tWT gene was present only in one fecal strain. Prevalence of the papG seP gene (class II variant) and prsG tWT gene (class III variant) was not signi¢- cantly di¡erent between the cystitis and pyelonephritis strains, unlike other studies showing that the papG seP gene predominates in pyelonephritis strains while the prsG tWT gene is most frequent in cystitis strains [3]. However, the statistical analysis of our data showed that papG seP was associated with higher relative virulence than prsG tWT in the strains isolated from pyelonephritis.…”

Section: Discussioncontrasting

confidence: 87%

“…P ¢mbriae have three de¢ned PapG adhesin variants; class I variant encoded by the papG tWT gene, class II variant (P adhesin) encoded by the papG seP gene and class III variant (F adhesin) encoded by the prsG tWT gene [2]. It has been shown that P adhesin predominates in acute pyelonephritis strains, while F adhesin is most frequent in cystitis strains [3]. F1C ¢mbriae (encoded by the foc operon) are genetically related to S ¢mbriae and their nucleotide sequences share a high degree of homology [4,5].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Identification of S, F1C and three PapG fimbrial adhesins in uropathogenic Escherichia coli by polymerase chain reaction

Mitsumori¹

1998

FEMS Immunology and Medical Microbiology

View full text Add to dashboard Cite

S and F1C fimbrial adhesins often expressed by uropathogenic Escherichia coli are genetically homologous. A multiply primed polymerase chain reaction (PCR) was developed for discriminating the S (sfa) and F1C (foc) fimbrial operons. A total of 270 uropathogenic E coli strains and 80 fecal isolates were examined. PCR specifically detected the sfa and foc alleles in 105 (93%) of 113 sfa/foc+ strains by DNA hybridization. Furthermore, 87% of sfa+ uropathogenic E. coli simultaneously possessed the genes encoding the class III P fimbrial adhesin (prsG(J96)), alpha-hemolysin and cytotoxic necrotizing factor 1. Statistical analysis showed the class II P fimbrial adhesin (papG(IA2)) and F1C fimbria to be associated with high relative virulence in pyelonephritis and cystitis, respectively. The multiply primed PCR developed should be useful for assessing the contribution of the S and F1C fimbriae in the pathogenesis of urinary tract infections.

show abstract

Section: Discussioncontrasting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Identification of S, F1C and three PapG fimbrial adhesins in uropathogenic Escherichia coli by polymerase chain reaction

Mitsumori¹

1998

FEMS Immunology and Medical Microbiology

View full text Add to dashboard Cite

show abstract

“…Another constructed DNA probe, named drb (130), was a 260-bp PstI fragment of plasmid pIL14 (afa-1 operon) coding for the AfaE-I adhesin expressed by the uropathogenic Afa/Dr DAEC KS52 strain (243). This DNA probe has been used in epidemiological studies of the associ-ation of Afa/Dr DAEC with urinary tract infection (13,130,131,250,287,466,467). The results show a high positive correlation of the colony hybridization assay with the adhesion assay and the hemagglutination inhibition assay described above.…”

Section: Diagnosismentioning

confidence: 99%

Pathogenesis of Afa/Dr Diffusely AdheringEscherichia coli

2005

View full text Add to dashboard Cite

Over the last few years, dramatic increases in our knowledge about diffusely adhering Escherichia coli (DAEC) pathogenesis have taken place. The typical class of DAEC includes E. coli strains harboring AfaE-I, AfaE-II, AfaE-III, AfaE-V, Dr, Dr-II, F1845, and NFA-I adhesins (Afa/Dr DAEC); these strains (i) have an identical genetic organization and (ii) allow binding to human decay-accelerating factor (DAF) (Afa/DrDAF subclass) or carcinoembryonic antigen (CEA) (Afa/DrCEA subclass). The atypical class of DAEC includes two subclasses of strains; the atypical subclass 1 includes E. coli strains that express AfaE-VII, AfaE-VIII, AAF-I, AAF-II, and AAF-III adhesins, which (i) have an identical genetic organization and (ii) do not bind to human DAF, and the atypical subclass 2 includes E. coli strains that harbor Afa/Dr adhesins or others adhesins promoting diffuse adhesion, together with pathogenicity islands such as the LEE pathogenicity island (DA-EPEC). In this review, the focus is on Afa/Dr DAEC strains that have been found to be associated with urinary tract infections and with enteric infection. The review aims to provide a broad overview and update of the virulence aspects of these intriguing pathogens. Epidemiological studies, diagnostic techniques, characteristic molecular features of Afa/Dr operons, and the respective role of Afa/Dr adhesins and invasins in pathogenesis are described. Following the recognition of membrane-bound receptors, including type IV collagen, DAF, CEACAM1, CEA, and CEACAM6, by Afa/Dr adhesins, activation of signal transduction pathways leads to structural and functional injuries at brush border and junctional domains and to proinflammatory responses in polarized intestinal cells. In addition, uropathogenic Afa/Dr DAEC strains, following recognition of β1 integrin as a receptor, enter epithelial cells by a zipper-like, raft- and microtubule-dependent mechanism. Finally, the presence of other, unknown virulence factors and the way that an Afa/Dr DAEC strain emerges from the human intestinal microbiota as a “silent pathogen” are discussed

show abstract

“…afaBC/daaC positivity has been found in UPEC strains belonging to the B2 phylogroups (61). Epidemiological studies show that E. coli isolates expressing Afa/Dr adhesins are involved in cystitis in children (25 to 50%) and pyelonephritis in pregnant women (30%) (34,53,(55)(56)(57)(84)(85)(86)(87)(88)(89)(90)(91)(92)(93). In addition, these pathogenic E. coli strains cause UTIs in pregnant women (30,90,91,(94)(95)(96)(97).…”

Section: Urinary Tract Infectionsmentioning

confidence: 99%

Pathogenesis of Human Diffusely Adhering Escherichia coli Expressing Afa/Dr Adhesins (Afa/Dr DAEC): Current Insights and Future Challenges

Servin

2014

Clin Microbiol Rev

View full text Add to dashboard Cite

SUMMARY The pathogenicity and clinical pertinence of diffusely adhering Escherichia coli expressing the Afa/Dr adhesins (Afa/Dr DAEC) in urinary tract infections (UTIs) and pregnancy complications are well established. In contrast, the implication of intestinal Afa/Dr DAEC in diarrhea is still under debate. These strains are age dependently involved in diarrhea in children, are apparently not involved in diarrhea in adults, and can also be asymptomatic intestinal microbiota strains in children and adult. This comprehensive review analyzes the epidemiology and diagnosis and highlights recent progress which has improved the understanding of Afa/Dr DAEC pathogenesis. Here, I summarize the roles of Afa/Dr DAEC virulence factors, including Afa/Dr adhesins, flagella, Sat toxin, and pks island products, in the development of specific mechanisms of pathogenicity. In intestinal epithelial polarized cells, the Afa/Dr adhesins trigger cell membrane receptor clustering and activation of the linked cell signaling pathways, promote structural and functional cell lesions and injuries in intestinal barrier, induce proinflammatory responses, create angiogenesis, instigate epithelial-mesenchymal transition-like events, and lead to pks -dependent DNA damage. UTI-associated Afa/Dr DAEC strains, following adhesin-membrane receptor cell interactions and activation of associated lipid raft-dependent cell signaling pathways, internalize in a microtubule-dependent manner within urinary tract epithelial cells, develop a particular intracellular lifestyle, and trigger a toxin-dependent cell detachment. In response to Afa/Dr DAEC infection, the host epithelial cells generate antibacterial defense responses. Finally, I discuss a hypothetical role of intestinal Afa/Dr DAEC strains that can act as “silent pathogens” with the capacity to emerge as “pathobionts” for the development of inflammatory bowel disease and intestinal carcinogenesis.

show abstract

Molecular epidemiology of adhesin and hemolysin virulence factors among uropathogenic Escherichia coli

Cited by 160 publications

References 33 publications

Identification of S, F1C and three PapG fimbrial adhesins in uropathogenic Escherichia coli by polymerase chain reaction

Identification of S, F1C and three PapG fimbrial adhesins in uropathogenic Escherichia coli by polymerase chain reaction

Pathogenesis of Afa/Dr Diffusely AdheringEscherichia coli

Pathogenesis of Human Diffusely Adhering Escherichia coli Expressing Afa/Dr Adhesins (Afa/Dr DAEC): Current Insights and Future Challenges

Contact Info

Product

Resources

About