What is the significance and prevalence of the fliCD and satF genes in uropathogenic Escherichia coli?

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Significance and Prevalence of fliCD and satF Genes in UPEC

The fliCD gene is highly prevalent (90%) in UPEC clinical isolates and is critical for flagellar-mediated motility and pathogenesis, while the satF gene (encoding Sat toxin) represents a significant virulence determinant associated with acute pyelonephritis that causes vacuolating cytotoxicity in bladder and kidney epithelial cells.

fliCD Gene: Flagellar Biosynthesis and Motility

Prevalence and Clinical Significance

  • The fliCD gene was detected in 90% of UPEC clinical isolates from women with UTIs, making it one of the most prevalent virulence genes after fimH (100%) 1
  • This high prevalence correlates with the observation that 98% of clinical UPEC isolates demonstrated motility phenotypes, indicating functional flagellar expression 1

Functional Role in Pathogenesis

  • The fliCD genes are essential for flagellar biosynthesis and assembly, representing structural components required for complete flagellar formation 2
  • Motility conferred by functional flagella enables UPEC to ascend the urinary tract, facilitating colonization of upper urinary tract sites and contributing to both lower and upper UTI pathogenesis 1
  • The strong association with phylogenetic group B2 (the most prevalent group in this UPEC cohort) suggests fliCD is part of the core virulence repertoire of highly pathogenic extraintestinal E. coli 1

satF Gene: Secreted Autotransporter Toxin

Clinical Association and Prevalence

  • The Sat protein (encoded by satF) is expressed significantly more often by E. coli strains causing acute pyelonephritis compared to fecal commensal strains (P = 0.029), establishing its role as a pathogenicity marker 3
  • Sat represents a 107 kDa serine protease autotransporter toxin that belongs to the SPATE (serine protease autotransporters of Enterobacteriaceae) family 3

Mechanism of Pathogenicity

  • Sat functions as a vacuolating cytotoxin specifically targeting bladder and kidney epithelial cells, causing cellular elongation, loosening of cellular junctions, and significant cytoplasmic vacuolation 4
  • In murine models of ascending UTI, Sat causes dissolution of glomerular membranes and vacuolation of proximal tubule cells during upper urinary tract infection 4
  • Sat-deficient mutants produced no histological kidney damage compared to wild-type UPEC CFT073, demonstrating that Sat directly contributes to tissue pathology rather than bacterial burden 4

Immunogenic Properties

  • Sat elicits a strong antibody response during infection, as demonstrated by detection of Sat antibodies in sera of mice infected with UPEC CFT073 3
  • This immunogenicity, combined with its cytopathic phenotype and association with pathogenic isolates, confirms Sat as a bona fide virulence determinant 3

Clinical Implications

Diagnostic Considerations

  • The high prevalence of fliCD (90%) in UPEC isolates suggests that motility assessment could serve as a rapid phenotypic screening tool for uropathogenic potential 1
  • The presence of bacterial morphotypes in urine sediment (observed in 65% of UPEC-positive samples) should be incorporated into routine urinalysis procedures as it correlates with virulence gene carriage 1

Pathogenic Potential

  • UPEC isolates carrying both fliCD and satF genes possess the molecular machinery for both ascending colonization (via motility) and direct tissue damage (via cytotoxicity), indicating capacity to cause complicated upper UTI and recurrent infections 1, 4
  • The combination of high biofilm formation (100%), motility (98%), and cytotoxin production positions these strains for persistent and recurrent UTI 1

References

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