Urinary Tract Infection, UTI - Virulence factors, Uropathogenic E. coli, UPEC
Virulence factors of UPEC (Uropathogenic E. coli)
The virulence factors of UPEC (Uropathogenic E. coli), the causative agent of Urinary Tract Infection (UTI), include:
Type 1 fimbriae that bind to uroepithelial cells
Type P fimbriae that recognize kidney glycosphingolipids
Siderophores that help gather iron from the host
α and β-hemolysins that lyse host erythrocytes
Capsules
Sat protein that acts as a proteolytic toxin
These virulence factors include increased adherence to vaginal and uroepithelial cells by bacterial surface structures (adhesins, in particular, pili). The alpha-hemolysin is produced and resistance to serum-killing activity occurs.
UPEC has pathogenicity islands encoded in its genes (eg. hemolysins and E. coli, Proteus fimbriae). Pathogenicity islands contain genes that are associated with virulence and are absent from avirulent or less virulent strains of the same species
Adherence is an important virulence factor to cause UTIs such as Proteus. Proteus strains can uniquely adhere to the mucosa of kidneys. Also, Proteus can produce urease, hydrolyzing urea Hydrolysis of urea which increases the pH of urine (urine pH) that are directly toxic to kidney cells and can also form kidney stones. The same is the case with Klebsiella spp.
Staphylococcus saprophyticus also adheres better to uroepithelial cells than does Staphylococcus aureus or Staphylococcus epidermidis.
Other bacterial characteristics also contribute to virulence factors such as motility (ascending to the upper tract against the flow of urine) and cause pyelonephritis.
Some organisms demonstrate the production of K-antigen (capsule or outer cell wall). This antigen protects bacteria from being phagocytosed.
Despite numerous host defenses and even antibiotic treatment, recurrent UTIs can be observed in high proportions.
Some studies have shown that uropathogens can invade superficial epithelial cells in the bladder and replicate, forming large foci of intracellular E. coli.
This invasion triggers the host's immune responses which in turn causes the superficial cells to exfoliate within hours of infection.
Intracellular microorganisms can re-emerge from the bladder epithelial cells and invade the underlying new superficial layer of epithelial cells.
Intracellular bacteria mature into numerous, large protrusions on the bladder surface they refer to as ‘pods’. In such “pods”, the intracellular bacteria are embedded in a fibrous, polysaccharide-rich matrix resembling that of a biofilm. The prevalence of “pods” may further help explain the persistence of bladder infections despite strong host defenses.