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MBB 328 > Lecture 18 - E Coli > Flashcards

Lecture 18 - E Coli Flashcards

1
Q

Classification?

A

Gram-negative rod

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2
Q

How do non-pathogenic E Coli become pathogenic?

A

Acquire virulence genes via natural transformation, transduction and conjugation.

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3
Q

Diseases caused?

A

Diarrhea, dysentary, UTI, hemolytic uremic syndrome (kidney failure), sepsis, pneumonia and meningitis

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4
Q

What are the serological classes of E Coli? What is the system based on?

A

O (of LPS), H (flagellar), K (capsule). Based on reactivity of surface antigens to different antibodies.

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5
Q

What are the two pathotypes of E Coli?

A

Diarrheagenic and extraintestinal

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6
Q

How do E Coli infect their host?

A

Fecal-oral route, attach to intestinal mucosa via different types of pili/fimbrae

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7
Q

How does death most commonly occur during E Coli infection? What is the best treatment?

A

Dehydration. Drink water, rather than take antibiotics.

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8
Q

What are the virulence genes encoded by E Coli?

A 
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
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9
Q

What are pili and how are they used by E Coli?

A 
Pili/fimbriae: long thin surfacedisplayed
polymers of pilin
subunits.
Most pili are involved in
adhesion to host receptors.
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10
Q

What are unique properties of Type IV pili?

A 
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.
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11
Q

What is EPEC?

A

Enteropathogenic E Coli. Food-borne, water-borne outbreaks in developing countries (contamination of food and water due to poor sanitation infrastructure)

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12
Q

What are attaching and effacing lesions?

A

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

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13
Q

What is A/E caused by?

A

Gene products of the mobile genetic element LEE (Locus

of Enterocyte Effacement): Tir, T3SS, intimin, effectors)

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14
Q

How is A/E initiated?

A 
Type IV pilus– the “bundle
forming pilus” (BFP) to aggregate and
form “microcolonies”, and for initial
adherence to epithelial cells of the
small intestine
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15
Q

What is injected into the host via T3SS and what does this result in?

A

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

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16
Q

Which pathogens that we have covered have T3S systems? How do so many pathogens encode for this?

A

EPEC, EHEC, P. aeruginosa. Horizontal gene transfer via mobile genetic elements.

17
Q

What is effacement?

A

Loss of microvilli means loss of absorptive surface

18
Q

How do EPEC T3SS effectors cause diarrhea and dehydration?

A

Disrupt water absorption and ion balance, activate ion secretion, disrupt epithelial tight junctions to increase intestinal permeability, inflammation -> water/electrolyte loss

19
Q

What is EspA?

A 
Early T3S effector protein –
is translocated through the T3S
needle and forms and extracellular
filament (translocation tube)through which other
effectors are translocated
20
Q

What is Esp B, EspD?

A

Early T3S effectors –
form a pore in the host cell
membrane – the translocon – that
the needle interacts with.

21
Q

What is Tir?

A 
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
22
Q

Which host cell machinery is responsible for pedestal formation and how does it achieve this?

A

Binding of Nck and recruitment and activation of N-WASP and the Arp2/3 complex and actin
filament formation that causes pedestal formation

23
Q

What diseases and symptoms are caused by EHEC?

A

“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.

24
Q

EHEC virulence factors?

A

-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

25
Q

What diseases and symptoms are caused by ETEC?

A

Causes watery diarrhea in infants and “Traveller’s

Diarrhea”; mostly a problem in developing countries.

26
Q

ETEC virulence factors?

A
  • fimbrial adhesins e.g. CFA I, CFAII, CFA/III (a type IV
    pilus), CS1, 3, 6 etc.
  • produces heat labile toxin (LT) and/or heat stable toxin
    (ST)
  • non-invasive
27
Q

What is the structure of Shigatoxin (Stx)?

A

-Is an AB5 toxin
- five identical B subunits bind to glycolipid
globotrialosylceramide (Gb3) on epithelial cells
- A subunit is the catalytic subunit – a glycosidase -
interacts w/ ribosomes and cleaves ribosomal RNA,
disrupting protein synthesis -> cell death (recognizes
and cleaves a specific adenine base on the 28S RNA of
the 60S ribosomal subunit)

28
Q

What are LT?

A

Heat-labile AB5 enterotoxin - activity is lost after 30 min inc’n at 100 oC
- ADP-ribosylating enzyme
- B subunits bind to GM1 on intestinal epithelial cells
- A subunit is an ADP ribolysating enzyme - covalently attaches ADP
ribose (ADPR) to the stimulatory G protein Gsa

29
Q

What are ST?

A

Heat-stable enterotoxin – activity retained after 30 min at 100 oC
- two types: STa and STb - small peptide toxins
- STa binds to guanylate cyclase on host cell membranes – binding
stimulates production of intracellular cGMP

30
Q

What do LT and ST have in common?

A

Both toxins lead to opening of CFTR chloride channel – ions/H2O are
released, fluid uptake is inhibited -> net fluid loss -> diarrhea

31
Q

What does pili bind to on the host cell?

A

Microvilli

32
Q

Where does EPEC, EHEC and ETEC cause disease?

A

EPEC - small intestine
EHEC - large intestine
ETEC - small intestine

MBB 328 (10 decks)

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