Disease relevance of sfa

• The Escherichia coli operons daa and sfa encode F1845 and S pili, respectively [1].
• With the exception of small alterations in the sfa-coding region the genetic determinants for S fimbriae were identical in uropathogenic O6:K+ and meningitis O18:K1 and O83:K1 strains [2].
• These results suggest that the hly, kps, sfa, and pap pathogenicity determinants may play a role in the evolution of enteric bacteria quite apart from, and perhaps with precedence over, their ability to cause disease [3].

High impact information on sfa

• Deletion of this pathogenicity island (paill) not only removes the hly- and prf-specific genes, but also represses S fimbriae (Sfa), although the sfa genes of this virulence factor are not located on paill [4].
• We also show that Lrp binds to the daa and sfa regulatory regions and that this binding is modulated by the methylation of the GATC sites [1].
• Surprisingly, other fimbrial genes, such as pap and foc/sfa, and genes involved in motility and chemotaxis were downregulated in vivo [5].
• The isolates within these virulent lineages typically carried DNA homologous to the adhesin operon pap or sfa and the hemolysin operon hly and expressed O1, O2, O4, O6, O18, O25, or O75 antigens [6].
• Structure and copy number analyses of pap-, sfa-, and afa-related gene clusters in F165-positive bovine and porcine Escherichia coli isolates [7].

Chemical compound and disease context of sfa

• Leucine-responsive regulatory protein and deoxyadenosine methylase control the phase variation and expression of the sfa and daa pili operons in Escherichia coli [1].
• Probes from different segments of the pap, sfa, and afaI operons were used in Southern hybridization to analyze 18 F165-positive, mannose-resistant hemagglutinating E. coli isolates possessing pap- and sfa-, pap- and afa-, or pap-related sequences [7].
• The multiplex PCR to detect pap, sfa, afaI, hly, aer and cnf1 genes was highly specific and the sensitivity was found to be about 5 x 10(3) colony forming units of E. coli per ml [8].

Biological context of sfa

• Only one copy of the sfa determinant was identified on the chromosome of these strains [2].
• By restriction analysis and by DNA-DNA hybridization, it could be shown that the cloned fimbrial determinant of strain BK658 exhibits a high degree of sequence homology to the gene clusters coding for S fimbrial adhesins (sfa) and F1C fimbriae (foc) [9].
• The reintroduction of the cloned S fimbrial adhesin determinant (sfa) increases the virulence of the avirulent mutant strain by a factor of 20; almost the same effect was observed after restoration of serum resistance by integration of an sfa+ recombinant cosmid into the chromosome [10].
• It is shown that the Sfa-negative phenotype is due to a block in transcription of the sfa genes [11].
• In the biogenesis of S fimbriae, the proteins encoded by the sfa genes are presumably required in a specific stoichiometry [12].

Anatomical context of sfa

• Analysis of the genetic determinants coding for the S-fimbrial adhesin (sfa) in different Escherichia coli strains causing meningitis or urinary tract infections [2].
• Certain F165-positive isolates sharing similar DNA sequences with both pap and sfa operon sequences demonstrated mannose-resistant hemagglutination of sheep erythrocytes, as observed in human uropathogenic E. coli possessing the prs operon [13].
• Four different gene clusters have been characterized so far which encode adhesins involved in the specific binding of pathogenic Escherichia coli to epithelial cells of the urinary tractus: the pap, sfa, afa and bma operons [14].
• Although less frequently, genes encoding these VFs especially pap, sfa, hly, and cnf 1 genes were also associated with E. coli strains isolated from feces of healthy cats, in contrast to the distribution pattern of uropathogenic E. coli observed in humans [15].

Associations of sfa with chemical compounds

• However, the loss of the inserts not only affected the hemolytic phenotype but led to a considerable reduction in serum resistance and the loss of mannose-resistant hemagglutination, caused by the presence of S-type fimbriae (sfa) [11].
• Virulence gene frequencies detected in those isolates which had been randomly collected (68 canine strains) were: 43% pap, 57% sfa, 1% afa, 44% hly, 41% cnf1 and 34% aer [16].

Other interactions of sfa

• Comparison of the genetic determinant coding for the S-fimbrial adhesin (sfa) of Escherichia coli to other chromosomally encoded fimbrial determinants [17].

Analytical, diagnostic and therapeutic context of sfa

• Rapid and specific detection of the pap, afa, and sfa adhesin-encoding operons in uropathogenic Escherichia coli strains by polymerase chain reaction [18].
• Southern hybridizations with specific sfa probes, following pulsed-field gel electrophoresis (PFGE), showed positive hybridization to the same fragment in each of these strains [19].
• Southern blot analysis of the S fimbrial adhesin (sfa) determinants of normal and hyper-fimbriated strains revealed no marked difference in the gene structure [20].

References