Other Virulence Determinants of UPEC
UPEC employs multiple virulence mechanisms beyond adhesins that enable survival, persistence, and pathogenicity in the urinary tract, including biofilm formation, serum resistance, capsular protection, and autotransporter-mediated adherence.
Biofilm-Associated Genes
Biofilm formation represents a critical virulence mechanism that allows UPEC to establish persistent infections and evade host defenses:
Approximately 84% of UPEC strains are moderate to strong biofilm producers, making this a dominant pathogenic trait 1.
Specific adhesin genes correlate with enhanced biofilm formation, particularly papAH (P fimbriae), bmaE (M fimbriae), and sfaS (S-fimbriae), which show higher prevalence in moderate to strong biofilm-producing strains 1.
The pap adhesin gene demonstrates significant correlation with biofilm production (p ≤ 0.05), and among multidrug-resistant UPEC strains, 54% are biofilm producers 2.
Phenotypic expression of type 1 fimbriae (fimH gene present in 91.8% of UPEC) is directly associated with biofilm formation, while P fimbriae expression shows no such association 1, 2.
The autotransporter protein UpaC specifically mediates increased biofilm formation when expressed, representing an alternative biofilm-promoting mechanism 3.
Clinical Pitfall
The high prevalence of biofilm formation among multidrug-resistant strains creates a double threat—biofilms protect bacteria from both antibiotics and immune clearance, necessitating more aggressive or prolonged treatment strategies 2.
Serum Resistance Genes
While not extensively detailed in the provided evidence, serum resistance mechanisms allow UPEC to survive in bloodstream and tissue environments:
The traT gene, identified in 47.6% of hybrid UPEC strains, encodes an outer membrane protein that confers complement resistance 4.
Serum resistance enables UPEC to cause ascending infections and potentially progress to pyelonephritis or bacteremia 5.
Capsular Polysaccharides
Capsular structures provide multiple protective functions:
Capsules shield UPEC from phagocytosis and complement-mediated killing, representing a key defense against innate immunity 5.
The chuA gene (present in 57.1% of hybrid strains) is associated with capsule-related functions and iron acquisition, both contributing to survival in the urinary tract 4.
Capsular polysaccharides interfere with antibody binding and reduce bacterial surface hydrophobicity, preventing recognition by host defenses 5.
Autotransporter Proteins
Autotransporters represent a distinct class of surface-exposed virulence factors with diverse functions:
The prototype UPEC strain CFT073 contains 11 putative autotransporter-encoding genes, indicating the importance of this protein family 3.
UpaB mediates adherence to multiple extracellular matrix (ECM) proteins and is critical for early bladder colonization—CFT073 significantly outcompetes its upaB mutant in mouse bladder colonization experiments 3.
UpaB expression is constitutive in CFT073, while UpaC is transcriptionally repressed by the global regulator H-NS, suggesting differential regulation based on environmental conditions 3.
Autotransporters are common across E. coli strains, with upaB and upaC genes frequently detected by PCR screening, indicating their evolutionary conservation 3.
Mechanistic Insight
Autotransporters function independently of fimbrial adhesins, providing UPEC with redundant attachment mechanisms that ensure colonization even when primary adhesins are blocked or non-functional 3, 5.
Integration of Virulence Factors
UPEC demonstrates remarkable genetic plasticity, with hybrid strains carrying both uropathogenic and intestinal pathogenic E. coli virulence markers (10.5% of isolates), showing genetic diversity without belonging to particular clonal lineages 4.
The most commonly identified virulence genes across UPEC populations include fimH (71.5-91.8%), fyuA (66.7%), iutA (62%), and chuA (57.1%), representing iron acquisition and adhesion systems 2, 4.
Phylogenetic group B2 strains (58.7% of UPEC) show higher frequencies of both adhesin genes and antibiotic resistance, indicating that certain lineages have accumulated multiple virulence determinants 2.