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Bacteriology > Lecture 20 - E. Coli > Flashcards

Lecture 20 - E. Coli Flashcards

1
Q 
Ways to subtype E coli
1)
2)
3)
4)
5)
A

1) Serogroup/serotype
2) Multilocus sequence typing
3) Phage type
4) Pulsotype
5) Pathotype

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2
Q

What is the difference between serogroup and serotype?

A

Serogroup refers to O antigen

Serotype refers to H antigen

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3
Q

What gives the pulsotype?

A

RFLP of E coli genome

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4
Q

What is slowly replacing serotyping?

A

Multilocus sequence typing.

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5
Q

Multilocus sequence typing
1)
2)

A

1) Core genome clasification, not based on virulence factors

2) Sequence genes found in all E coli, compare them

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6
Q

Problem with serotyping

A

O, H antisera are required. These are expensive, produced in rabbits, so not completely accurate

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7
Q

What is phage typing used for?

A

Further defining serotypes of interest

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8
Q

What is pathotype based on?

A

Accessory genome

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9
Q

What can’t be pathotyped?

A

Opportunistic pathogens

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10
Q

Types of E coli causing intestinal infections

A

Primary pathogens

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11
Q

Types of E coli causing extra-intestinal infections

A

Opportunistic pathogens

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12
Q 
Examples of extra-intestinal infections caused by E coli
1)
2)
3)
4)
5)
6)
A

1) Urinary tract infection
2) Neonatal meningitis
3) Septicaemia
4) Wound infection
5) Peritonitis
6) Pneumonia

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13
Q

Most common G- cause of septicaemia

A

E coli

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14
Q

Most common G+ cause of septiicaemia

A

Staph aureus

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15
Q

Pilus that aids E coli in infecting the bladder

A

Type 1 pili

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16
Q

What do type 1 pili help E coli with?

A

Bladder colonisation

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17
Q

Type of pili that help E coli colonise the kidneys

A

Pap pili

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18
Q

What do pap pili help E coli with?

A

Colonisation of the kidneys

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19
Q

Which virulence determinant helps E coli survive in the blood?

A

Capsule (K type)

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20
Q

Most important K type

A

K1

Identical to capsule of Neisseria meningitidis type B (sialic acid)

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21
Q

Proportion of E coli causing septicaemia and meningitis with K1

A

80%

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22
Q 
Intestinal diseases caused by E coli
1)
2)
3)
4)
5)
6)
A

1) Non-specific infant diarrhoea
2) Traveller’s diarrhoea
3) Profuse watery diarrhoea
4) Dysentery
5) Haemorrhagic colitis
6) Diarrhoea-associated HUS

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23
Q

Haemolytic uremic syndrome symptoms
1)
2)
3)

A

1) Increased urea in blood
2) Erythrocyte lysis
3) Thrombocytopenia (low platelet count)

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24
Q

What is a neonate?

A

1st 28 days of life

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25
Q

MIcrobiological definition of an infant

A

Under 2 years of age

Some agents cause diarrhoea up until ~2 years

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26
Q 
Subtypes of diarrhoeogenic E coli 
1)
2)
3)
4)
5)
A

1) Enterotoxogenic E coli
2) Enteropathogenic E coli
3) Enterohaemorrhagic E coli
4) Enteroinvasive E coli
5) Enteroaggregative E coli

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27
Q

Another name for enteroinvasive E coli

A

Shigella

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28
Q

ETEC symptoms

A

Watery diarrhoea

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29
Q

EPEC symptoms

A

Non-specific diarrhoea in children

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30
Q

EHEC symptoms

A

Bloody diarrhoea, HUS

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31
Q

EIEC symptoms

A

Dysentery

32
Q

EAEC symptoms

A

Watery diarrhoea

33
Q

ETEC virulence factors
1)
2)
3)

A

1) Colonising factor antigen (CFA1)
2) Heat labile toxin
3) Heat stable toxin

34
Q

Requirements for ETEC to cause illness

A

Needs both CFA and a toxin gene (either LT or ST or both)

35
Q

Proportion of ETEC strains that only make ST

A

~1/3

36
Q

Proportion of ETEC strain that make both ST and LT

A

~1/2

37
Q

ETEC virulence factor in pigs

A

K88

38
Q

Proven ETEC human colonisation factors

A

CFA/1, CFA/2, CFA/4

39
Q

CFA/2 makeup

A

All have CS1 + either CS2 or CS3

40
Q

CFA/4 makeup

A

All have CS4 + either CS5 or CS6

41
Q 
Putative ETEC human colonisation factors
1)
2)
3)
4)
5)
6)
A

1) CS7
2) CS8
3) CS12
4) CS14
5) CS17
6) PCFO148

42
Q

What does CS3 attach to?

A

Microvili in the small intestine

Doesn’t cause damage or inflammation

43
Q

Which part of shigatoxin is an enzyme?

A

A1 subunit

44
Q

Heat labile toxin size

A

~86kD

45
Q

Heat stable toxin size

A

~2kD

46
Q

Heat labile toxin immunogenicity

A

High

47
Q

Why is heat stable toxin immunogenicity low?

A

Because it is too small a peptide to elicit a lymphocyte response

48
Q

Heat labile enterotoxin structure

A

AB5
Same structure as choleratoxin
A1 subunit is enzymatic

49
Q

Why is heat stable enterotoxin so stable?

A

It has 3 disulphide links in the space of quite a short primary structure

50
Q

Which hormone has the same mode of action as heat-stable enterotoxin?

A

Guanylin

51
Q

What is guanylin?

A

Hormone

Same action as heat-stable enterotoxin

52
Q

Why doesn’t guanylin cause pathology?

A

It only has two disulphide bonds, so it can be broken down by the body when not needed

53
Q

What does heat labile enterotoxin act via?

A

Cyclic AMP

54
Q

What does heat stable enterotoxin act via?

A

Cyclic GMP

55
Q

Which enterotoxin acts via cyclic GMP?

A

Heat stable

56
Q

Which enterotoxin acts via cyclic AMP

A

Heat labile

57
Q

Effect of heat stable and heat labile enterotoxins on gut

A

Increase Cl- secretion from crypts

Decrease NaCl absorption by vili

58
Q

Two-stage model of EPEC adherence
1)
2)

A

1) Plasmid-mediated. Bfp binds microvili

2) Chromosomal. Tir/intimin, attaching/effacing lesion

59
Q

EPEC pathogenicity island

A

LEE

Locus for enterocyte effacement pathogenicity island

60
Q

Locus for enterocyte effacement pathogenicity island contents

A

T3SS (EG: EspA)
Tir
Intimin
Effector proteins (EG: EspB, EspD)

61
Q 
EHEC virulence determinants
1)
2)
3)
4)
5)
6)
7)
A

1) Stx1
2) Stx2
3) Intimin
4) Efa
5) Secreted proteins (EspB)
6) Haemolysin
7) Serine protease (EspP)

62
Q

What encodes Stx1 in EHEC?

A

Phage

63
Q

What encodes Stx2 in EHEC?

A

Phage

64
Q

Can Stx2 be neutralised by anti-Stx1?

A

No

65
Q

Stx2 homology with Stx1

A

~60%

66
Q 
Shigatoxin processing
1)
2)
3)
4)
5)
A

1) Binds Gb3
2) Internalised into cell
3) In Golgi, broken into A and B subunits
4) In ER, broken into A1 and A2 subunits
5) A1 subunit binds 28S of 60S ribosomal subunit. Acts as a glycosidase.

67
Q

Broader category of pathogenic E coli that EHEC fits into

A

STEC (shigatoxin-producing E coli)

68
Q

Efa

A

EHEC factor for adhesion

69
Q

Difference between STEC and EHEC

A

STEC is an E coli that produces shigatoxin

EHEC is an STEC with additional virulence determinants, that can cause haemolytic uremic syndrome or haemolytic colitis

70
Q

Large E coli outbreak in Europe in 2011

A

E coli O104:H4

Enteroaggregative E coli

71
Q

Death toll from 2011 enteroaggregative E coli outbreak

A

50

72
Q 
EHEC pathogenesis
1)
2)
3)
4)
5)
6)
A

1) Bacteria ingested in food or water (faecal contamination)
2) Attach to intestinal mucosa
3) Produce shigatoxin
4) Toxins absorbed
5) Damage to small blood vessels supplying gut, kidney, pancreas, heart, brain
6) HUS occurs when there is intravascular thrombosis and haemolysis

73
Q 
Why does shigatoxin damage small blood vessels?
1)
2)
3)
4)
5)
A

1) Shigatoxin is absorbed into the bloodstream through gut wall
2) Toxin damages endothelial cells, which leads to clotting cascade
3) This causes an intravascular thrombosis
4) Red blood cells are shorn on firbin in clot, leading to haemolysis
5) This interferes with blood supply to gut, other organs

74
Q

How can kidneys be damaged by shigatoxin?

A

Kidney vasculature, nephrons have Gb3 receptors

75
Q

How can EHEC infection cause diabetes?

A

Pancreas has Gb3 receptors in it.

Shigatoxin can lead to pancreatic damage

76
Q

Is fragmented blood cells a symptom of many diseases?

A

No. Very uncommon.

Present in EHEC infections

77
Q

Which shigatoxin is thought to be more toxic?

A

Stx2

Bacteriology (29 decks)

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