Uropathogenic Escherichia coli (UPEC) strains cause 70 to 90% of community-acquired UTIs in an estimated 150 million individuals annually and about 40% of all nosocomial UTIs. A variety of virulence genes are associated with Escherichia coli mediated urinary tract infections.
Uropathogenic strains of Escherichia coli express distinctive bacterial properties, products, or structures (virulence factors) which help them to overcome host defenses and colonize or invade the urinary tract.
Compared to commensal E. coli, Uropathogenic E.coli are better adapted to the urethra, periurethra, and vagina and causes greater proportion of UTIs. In general, the more virulence factors a strain expresses, the more severe an infection it is able to cause.
Virulence factors of recognized importance in the pathogenesis of urinary tract infection (UTI) are:
- Adhesins (P fimbriae, certain other mannose-resistant adhesins, and type 1 fimbriae): By attaching to host structures, it avoids being swept along by the normal flow urine and eliminated. Attachment is a necessary first step in the colonization and a precedent to invasive infection in many situations.
- K antigen (capsular polysaccharide): They coat the cell, interfering with 0-antigen detection and protecting the cell from host defense mechanisms. Capsule has Antiphagocytic and anticomplementary activities. The degree of impairment of phagocytosis is proportional to the amount of polysaccharide
- Resistance to serum killing: Acidic capsular polysaccharides and the Kl capsule contribute to virulence by shielding bacteria from phagocytosis and possibly from serum killing, in part by blocking activation of the alternative complement pathway.
- Hemolysin: Cytolytic protein toxin that lyses erythrocytes of all mammals
- Aerobactin system: E.Coli uses Aerobactin to sequester Iron.