Infectious disease 4

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hemorrhagic E. coli colonizing the small bowel they sit on pedestals - which are
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hemorrhagic E. coli colonizing the small bowel they sit on pedestals - which are
lesions that are formed as a result of the colonization mechanism used by this pathogen.
E. coli is a common member of the microbiome of the intestine (colon)—estimated
10^6 per g feces in humans
E. coli is also a frequent cause of
intestinal (ex. colitis) and invasive (ex. UTI) diseases—some of which are life-threatening
While most strains of E. coli are opportunistic—
infections being acquired endogenously in compromised hosts,
some E. coli are obligate pathogens, and are acquired
exogenously or from non-human reservoirs (zoonotic)
Hemorrhagic E. coli maintains a non-human reservoir in
bovine
Hemorrhagic E. coli are indirectly transmitted by
fecal-oral a common source mechanism
colonization of the intestine in hemorrhagic E. coli leads to
bloody (hemorrhagic) diarrhea
The virulence factors that allow for colonization and hemorrhage by hemorrhagic E. coli are encoded on
laterally-acquired genetic elements
Hemorrhagic E. coli produces a toxin (shiga-toxin), which attacks intestine vascular tract leading to hemorrage from vascular into the lumen large bowel and also attacks the
kidney tissue which can lead to a life-threatening condition called HUS (hemolytic uremia syndrome)
All materials that can be transmitted laterally and can transmit virulence factors, if they move into a commensal e. coli they can change it froman avirulent version to a now virulent pathogenic E. coliEvolution of pathogenesis in E. Coli was through a process oflateral acquisition of virulence factorsmaterial that can be laterally transferred can includeTransposons, PAI- pathogenicity islands, Phage, PlasmidsThe E. coli type III secretion (T3S) system is encoded on a 36-kbp laterally-acquired pathogenicity island called thelocus of enterocyte effacement, LEE-LEE is required forcolonization of the gut by hemorrhagic E. coliLEE includesstructural and regulatory genes for T3Sloss of LEE genes leads toreduced colonizationEnterocyte -epithelial cell of small bowelStructure of T3S systems ismostly conservedE. coli mutated for LEE and T3S aredefective in colonizationHemorrhagic E. coli colonization requires interaction between theafimbrial adhesin intimin, and the cell receptor Tir—translocated intimin receptorBoth intimin adhesin and Tir receptor are encoded byE. coli!TIR - isa dimer that is imbedded in host membraneHow is the receptor encoded by e. coli but ends up imbedded in the host membrane?It uses a t3S to translocate TIR from inside of E. coli into host intestinal cells