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Microbiology - Quiz 2 > E. Coli > Flashcards

E. Coli Flashcards

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1
Q

Differentiate between commensal E. coli and enteropathogenic E. coli.

A

Commensal E. coli: part of normal intestinal microflora (0.1%)

  • -Make vitamin K and some B vitamins
  • -Protects against other pathogens at mucosa

E. coli intestinal pathogens are STRAINS that have acquired VIRULENCE FACTORS through horizontal gene transfer

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2
Q

Understand the processes involved in the “evolution” of a pathogen.

A

Evolve by HORIZONTAL GENE TRANSFER via..

  • -Phage
  • -Plasmids
  • -Transposons
  • -Gene loss
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3
Q

List the toxins secreted by each of the six E. coli strains discussed.

A 
EHEC: STX, hemolysins
ETEC: ST, LT
EPEC: no toxins
EAEC: hemolysins, EAST
EIEC: no toxins
DAEC: no toxins
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4
Q

List the shiga toxin-producing E. coli (1) and the diarrheagenic E. coli. (4)

A 
Shiga toxin-producing EC (STEC):
EnteroHemorrhagic EC (EHEC)
Diarrheagenic: (PATI-D)
EnteroPathogenic EC (EPEC)
EnteroAggregative EC (EAEC)
EnteroToxigenic EC (ETEC)
EnteroInvasive EC (EIEC)
Diffuse Adhering EC (DAEC)
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5
Q

What is the most common EHEC serogroup?

A

O157:H7

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6
Q

How is EHEC spread? What is its infectious dose?

A 
Foods:
--Undercooked/contaminated ground beef
--Leafy vegetables
--Unpasteurized apple cider/juice
--Raw-milk dairy products
Animals (house pets, petting zoos)
Person-to-person contact

Infectious dose: very low, 100

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7
Q

What are the clinical symptoms of EHEC?

A

Abdominal pain
Bloody diarrhea
**Hemolytic uremic syndrome - can -> renal failure

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8
Q

What are the symptoms of hemolytic uremic syndrome? (4) What causes it? How can it be treated?

A

Destruction of RBCs, damage to lining of vessel walls due to apoptosis/necrosis; hemolytic anemia; thrombocytopenia

Caused by shiga-like toxin (STX) from E. coli

NO antibiotics (increase toxin production)
Treat with fluid management to protect kidney
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9
Q

Briefly list the steps of EHEC pathogenicity.

A

EHEC cells remain extracellular in gut (no bacteremia) - TOXIN gets into bloodstream

  1. Attachment via common pillus -> effacement
  2. T3SS mediated change in host cells by injection of Tir -> Tir-Intimin binding -> tight interaction
  3. Actin polymerization and pedestal formation
  4. Release of HEMOLYSIN, SHIGA-like toxin, and other factors
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10
Q

Why can animals carry EHEC without getting sick?

A

Shiga toxin binds a host glycolypid that is different between cattle and humans

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11
Q

What does EPEC cause? How is it transmitted?

A 
Childhood diarrhea (MANY cases)
Transmitted person to person
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12
Q

What does ETEC cause? How is it transmitted?

A

Traveler’s diarrhea, esp. in infants in developing word

Food/water
Person to person

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13
Q

What E. coli type causes the most epidemics?

A

STECs

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14
Q

Describe how EHEC binds to the gut, including virulence determinant involved.

A

Uses E. coli common pilus (same as commensal E. coli)

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15
Q

What is the pathogenicity island in EHEC? What does it encode

A

LEE = Locus of Enterocyte Effacement

  • -Encodes T3SS and effectors
  • -Encodes Tir and Intimin
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16
Q

How does the T3SS in EHEC function?

A

Induced by many things, including contact with host cell

EspA = needle
EspB/D pass through needle to tip -> form pores in eukaryotic membrane for proteins to pass through

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17
Q

How is the attachment of the T3SS in EHEC to the host cell promoted? Why? (know this)

A

Promotes attachment by creating its own receptor:

  • -Injects TIR into host cell -> exposed on host cell surface
  • -Expresses INTIMIN on its own membrane
  • -Tir and Intimin interact with each other, binding tightly

Doesn’t have much time, needs to attach to wall as it is moving along - this helps it attach faster

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18
Q

What is effacement? What is another name for it? Why does it occur? What results?

A

Loss of host cell microvilli
AKA A/E lesions
Occurs because host cell reabsorbs microvilli in response to attachment of E. coli

Results in DIARRHEA: reduced microvilli -> reduced absorption

19
Q

What happens when EHEC is firmly attached to a host cell?

A

Once attached, -> actin polymerization -> changes in cell bio/structure of host cell -> pedestal formation (essential for virulence)

20
Q

How did EHEC get its shiga-like toxin?

A

Bacteriophage-mediation transduction

21
Q

What are the roles of the A and B subunits of Shiga-Like Toxin? (may not need to know)

A 
B = mediates toxin uptake by receptor binding
A = interferes with protein synthesis by messing with 28S rRNA
22
Q

List the virulence determinants in EHEC. (8)

A 
Common pilus
Shiga-like toxin
T3SS, Tir/Intimin
Hemolysin
Capsule (K-antigen)
LPS (-> inflammation)
Nutrient acquisition pathways
23
Q

What is the role of hemolysin in EHEC?

A

Pore-forming protein that inserts into host cell membranes -> lysis

24
Q

What is the commensal strain of E. coli?

A

K12

25
Q

What pathogenicity islands does EPEC have?

A

T3SS with Tir/Intimin binding (forms A/E lesions)
Bundle-forming pili (BFP) for adherence & formation of microcolonies on surface of cells
NO toxins known

26
Q

How does EPEC cause diarrhea?

A

Effacement from attachment to/microcolony formation on host cell -> decreased absorption

27
Q

What virulence factors does ETEC have? (3) How do they work?

A

Fimbriae: help colonize small intestine

Labile toxin (LT): similar to cholera toxin, -> watery, slightly bloody diarrhea
--Targets AC -> increased cAMP -> inhibition of CFTR -> increased Cl secretion, blocking of Na uptake -> loss of fluid and electrolytes

Stabile toxin (ST): -> stimulation of guanylate cyclase -> increased cGMP (similar outcome to that of LT)

28
Q

List the adhesins used by each of the six E. coli strains discussed.

A 
EHEC: Common pilus, A/E
ETEC: Fimbriae
EPEC: Bundle-forming pili, A/E
EAEC: forms biofilms
EIEC: nonfimbrial adhesins
DAEC: (not discussed)
29
Q

What disease is caused by EAEC? What virulence factors does it have?

A

More aggressive childhood diarrhea, but similar to EPEC

Hemolysins
EnteroAggregative Stable Toxin (EAST)
Pet (plasmid-encoded toxin)

30
Q

What disease does EIEC cause? How is it transmitted? What is different about it?

A

Watery diarrhea with blood and mucous
Transmitted via contaminated food

Invasive! Can polymerize actin behind it (like Shigella)

31
Q

What is the adherence pattern of DAEC?

A

Diffusely adhering!

32
Q

Briefly describe the O104:H4 epidemic.

A

Bloody diarrhea, lots of serious complications (with HUS)
Caused by EAEC that had picked up the Shiga-like toxin
—NOT by EHEC!
Carried by infected bean sprouts

33
Q

How is E. coli diagnosed?

A

Stool samples
Enrich in Gm- broth
PCR -> virulence factors
Toxin analysis

34
Q

E. coli: lactose test

A

Positive

35
Q

E. coli: Sorbitol MacConkey Agar

A

O157:H7 sorbitol negative (red)

Commensal E. coli sorbitol positive (black)

36
Q

How is EHEC diagnosed?

A

Sorbitol-MacConkey agar (red)
Immunoassay for Shiga toxin
PCR for virulence genes

37
Q

How is ETEC diagnosed?

A

PCR for virulence genes

38
Q

How is EPEC diagnosed?

A

PCR for virulence genes

Tissue culture assay for localized adherence

39
Q

How is EAEC diagnosed?

A

PCR for virulence genes

Tissue culture assay for aggregative adherence

40
Q

How is EIEC diagnosed?

A

PCR for virulence genes

41
Q

How is DAEC diagnosed?

A

Tissue culture assay for diffuse adherence

42
Q

How is ETEC treated?

A

For travelers:
Loperamide (may use with fluoroquinolones)
Azithromycin
Rifaximin

43
Q

How is EPEC treated?

A

Abx guided by susceptibility testing for sever/protracted cases

44
Q

How is EAEC treated?

A

Fluoroquinolones for travelers, HIV patients

Microbiology - Quiz 2 (10 decks)

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