Lecture 18 - E Coli Flashcards
Classification?
Gram-negative rod
How do non-pathogenic E Coli become pathogenic?
Acquire virulence genes via natural transformation, transduction and conjugation.
Diseases caused?
Diarrhea, dysentary, UTI, hemolytic uremic syndrome (kidney failure), sepsis, pneumonia and meningitis
What are the serological classes of E Coli? What is the system based on?
O (of LPS), H (flagellar), K (capsule). Based on reactivity of surface antigens to different antibodies.
What are the two pathotypes of E Coli?
Diarrheagenic and extraintestinal
How do E Coli infect their host?
Fecal-oral route, attach to intestinal mucosa via different types of pili/fimbrae
How does death most commonly occur during E Coli infection? What is the best treatment?
Dehydration. Drink water, rather than take antibiotics.
What are the virulence genes encoded by E Coli?
Tn - transposon PAI - pathogenicity island ST - heat stable toxin (enterotoxin) LT - heat labile toxin (enterotoxin) LEE - locus of enterocyte effacement (a PAI) UTI - urinary tract infection HUS - hemolytic uremic syndrome
What are pili and how are they used by E Coli?
Pili/fimbriae: long thin surfacedisplayed polymers of pilin subunits. Most pili are involved in adhesion to host receptors.
What are unique properties of Type IV pili?
The Type IV pili are unique in that they are retractile – can assemble, bind to surfaces or substrates and pull them into the cell or pull the bacteria along – adhesion, DNA uptake, twitching motility, gliding motility, secretion etc.
What is EPEC?
Enteropathogenic E Coli. Food-borne, water-borne outbreaks in developing countries (contamination of food and water due to poor sanitation infrastructure)
What are attaching and effacing lesions?
EPEC attach to host cells, induce loss of
microvilli (effacement) and cytoskeletal rearrangements to form pedestals
that interact intimately with the bacteria – cytoskeletal remodeling of host cells
What is A/E caused by?
Gene products of the mobile genetic element LEE (Locus
of Enterocyte Effacement): Tir, T3SS, intimin, effectors)
How is A/E initiated?
Type IV pilus– the “bundle forming pilus” (BFP) to aggregate and form “microcolonies”, and for initial adherence to epithelial cells of the small intestine
What is injected into the host via T3SS and what does this result in?
The T3SS injects effectors into
intestinal epithelial cells -> efflux of
water and electrolytes -> diarrhea. Also, A/E lesions caused by the effector proteins that are
Which pathogens that we have covered have T3S systems? How do so many pathogens encode for this?
EPEC, EHEC, P. aeruginosa. Horizontal gene transfer via mobile genetic elements.
What is effacement?
Loss of microvilli means loss of absorptive surface
How do EPEC T3SS effectors cause diarrhea and dehydration?
Disrupt water absorption and ion balance, activate ion secretion, disrupt epithelial tight junctions to increase intestinal permeability, inflammation -> water/electrolyte loss
What is EspA?
Early T3S effector protein – is translocated through the T3S needle and forms and extracellular filament (translocation tube)through which other effectors are translocated
What is Esp B, EspD?
Early T3S effectors –
form a pore in the host cell
membrane – the translocon – that
the needle interacts with.
What is Tir?
Translocated intimin receptor – another T3S effector - assembles on host cell membrane and binds to intimin on EPEC surface ® intimate interaction between EPEC and host cell, pedestal formation
Which host cell machinery is responsible for pedestal formation and how does it achieve this?
Binding of Nck and recruitment and activation of N-WASP and the Arp2/3 complex and actin
filament formation that causes pedestal formation
What diseases and symptoms are caused by EHEC?
“Hamburger disease” (strain O157:H7). Causes
watery, potentially severe bloody diarrhea, can lead to
hemorrhage, hemolytic uremic syndrome (HUS): death
by acute kidney failure, esp. in children and infants.
Occurs in developed countries.
EHEC virulence factors?
-uses E. coli common pilus (ECP) plus a non-fimbrial
adhesin, intimin, to attach to epithelial cells of the
large intestine
- has LEE - forms A/E lesions, induces pedestal
formation, uses T3SS, Tir
- releases shiga toxin (Stx/verotoxin)
- non-invasive
