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MM- Bacteria > Pathogenic E.coli > Flashcards

Pathogenic E.coli Flashcards

1
Q

E.coli family?

A

Enterobacteriaceae

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2
Q

E.coli genus?

A

Escherichia

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3
Q

What type of anaerobe is E.coli?

A

Facultative anaerobe

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4
Q

How many bacteria colonise humans?

A

10^13 - 10^14

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5
Q

Bacteria contribute how much to our body weight?

A

2kg

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6
Q

Two most dominant commensal phyla?

A

Bacteriodetes and firmicutes

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7
Q

Benefits of gut commensals?

A
  • Provide essential and non-essential amino acids
  • Direct and indirect colonisation resistance
  • Provide short chain fatty acids (SCFAs) such as butyrate which are used by the intestinal epithelial cells as a main fuel/energy source
  • Provide vitamins such as vitamin B12, Vitamin K, Riboflavin and Biotin
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8
Q

Non-pathogenic E.coli are the predominant?

A

Facultative anaerobe in the gut

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9
Q

Pathogenic E.coli that causes UTIs?

A

UPEC

Uropathogenic E.coli

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10
Q

Pathogenic E.coli that causes neonatal meningitis?

A

NMEC

Neonatal meningitis E.coli

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11
Q

Name all the pathogenic E.coli able to cause enteric/diarrhoeal disease?

A 
EAEC- Enteroaggregative E.coli
ETEC- Enterotoxigenic E.coli
EIEC- Enteroinvasive E.coli
EHEC- Enterohaemorrhagic E.coli
EPEC- Enteropathogenic E.coli
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12
Q

Which pathogenic E.coli is the main cause of traveller’s diarrhoea?

A

ETEC- Enterotoxigenic E.coli

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13
Q

Which pathogenic E.coli is the second most common cause of traveller’s E.coli?

A

EAEC- Enteroaggregative E.coli

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14
Q

How can pathogenic E.coli be categorised/serotyped?

A

Based on the O and H antigens

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15
Q

O antigen?

A

LPS antigen

Consists of many repeats of an oligosaccharide unit

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16
Q

H antigen?

A

Flagellar antigen

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17
Q

Describe the structure of the LPS?

A

Has a lipid A base
This is attached to a core region
The core is then attached to the O antigen

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18
Q

What is the O antigen?

A

Consists of many repeats of an oligosaccharide unit

Part of the LPS

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19
Q

What is LPS?

A

It is an endotoxin

It is lipopolysaccharide

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20
Q

How did pathogenic E.coli form?

A

Thought to have evolved from commensal E.coli

Through the loss and gain of genes

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21
Q

How many genes are conserved between pathogenic and commensal E.coli and what are these genes called?

A

~3000 genes

These genes are house-keeping genes and are conserved as they are essential

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22
Q

How can pathogenic E.coli be serotyped?

A

Based on the O and H antigens

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23
Q

What does pathogenic E.coli require to cause disease?

A
  • Access to the host
  • Must be able to colonise a surface in the host
  • Must be adapted to the environment it colonises
  • Must be able to obtain nutrients
  • Must be able to reproduce
  • Must be able to evade the host immune defences
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24
Q

Which enteric/diarrhoeal E.coli are extracellular?

A

EAEC
EHEC
EPEC
ETEC

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25
Q

Which of the enteric/diarrhoeal E.coli are intracellular invasive pathogens?

A

EIEC

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26
Q

How does the immune system recognise the bacteria, describe the TLRs?

A

TLR5 recognises flagellin
TLR4 recognises LPS of gram negative bacteria
TLR2 recognises gram positive bacteria

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27
Q

TLRs 5,2,4 signal via

A

Myd88 which induces NF-kB

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28
Q

UPEC is the most common cause of?

A

Nosocomial and community acquired UTIs

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29
Q

UPEC colonisation factors?

A

Type I pili
P pili
S pili

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30
Q

Type I pili are used by UPEC to colonise?

A

The bladder

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31
Q

Type P pili are used by UPEC to colonise?

A

The kidney

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32
Q

What toxins/virulence determinants are produced by UPEC?

A

HlyA
CNF1
Sat toxin

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33
Q

What does UPEC HlyA do?

A

It is an alpha haemolysin
It is a pore forming toxin
Can form pores in e.g. neutrophils to induce cell death

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34
Q

What does UPEC CNF1 do?

A

It an inhibit phagocytosis

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35
Q

What does UPEC Sat toxin do?

A

Can lead to urothelial cell exfoliation

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36
Q

What is UPEC Sat toxin?

A

It is a SPATE

Serine Protease Autotransporter of Enterobacteriaceae

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37
Q

What are SPATEs?

A

Serine Protease Autotransporters of Enterobacteriaceae

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38
Q

What are some siderophores of UPEC?

A

IroN
IreA
Aerobactin

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39
Q

What do siderophores bind to?

A

Ferric (Fe3+) iron

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40
Q

EIEC has the same method of infection as?

A

Shigella

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41
Q

Which pathogenic E.coli are T3SS dependent?

A

EHEC
EPEC
EIEC

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42
Q

Which pathogenic E.coli are T3SS independent?

A

ETEC

EAEC

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43
Q

EAEC is the second most common cause of?

A

Traveller’s diarrhoea

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44
Q

EAEC colonises where?

A

Ileum of the small intestine

Large intestine/colon

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45
Q

Symptoms of EAEC infection?

A

Watery diarrhoea with or without the presence of mucus/blood

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46
Q

Treatment of EAEC?

A

Rehydration therapy
Self limiting- should get better without treatment
Although antibiotics can be given to speed up recovery

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47
Q

Why is EAEC known as aggregative E.coli?

A

Due to the characteristic aggregative adherence structure it forms

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48
Q

Three stages of EAEC pathogenesis?

A

1) Colonisation via AAF (aggregative adherence fimbriae)
2) Biofilm formation
3) Release of toxins and elicitation of an inflammatory response, mucosal toxicity, and intestinal secretion

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49
Q

What is the colonisation factor of EAEC?

A

AAF which is aggregative adherence fimbriae

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50
Q

How do the aggregates form?

A

Through the bacteria binding to the epithelial cell surface and through binding to each other

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51
Q

What promotes expression of AAF?

A

AggR transcription regulator

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52
Q

EnteroaggregativeEscherichia coli(EAEC) adherence to human intestinal tissue is mediated by?

A

AAF = aggregative adherence fimbriae

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53
Q

What are key virulence determinants of EAEC?

A

SPATEs= Pic and Pet
EAST-1
ShET1

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54
Q

What are SPATEs?

A

Serine protease autotransporters of Enterobacteriaceae

55
Q

What are the SPATEs important in EAEC virulence?

A

Pet and Pic

56
Q

How are Pet and Pic secreted?

A

Via the T5SS: Type V secretion system

57
Q

What is Pet?

A

Plasmid encoded toxin

58
Q

What does Pet do?

A

Interferes with cytoskeleton integrity and results in cell death

59
Q

What does Pic do?

A

Involved in intestinal colonisation
It is a mucinase
Allows penetration through the mucus layer

60
Q

What is Pic?

A

It is a mucinase

Allows contact with the epithelium by allowing penetration through the mucus layer

61
Q

How does EAEC cause watery diarrhoea?

A

EAST1

ShET1

62
Q

What does EAST1 do?

A

This toxin causes increased secretion of chloride and has been associated with secretory diarrhoea

63
Q

When was the EAEC outbreak in Germany?

A

2011

64
Q

How many people died in the EAEC outbreak in Germany?

A

~50

65
Q

What was the serotype of the EAEC that caused the outbreak in Germany?

A

O104:H4

66
Q

Why was O104:H4 EAEC so deadly?

A

It was an enteroaggregative E.coli that was able to produce Shiga toxin. This made it an excellent and very virulent coloniser.

67
Q

ETEC colonises which part of the body?

A

The small intestine

68
Q

ETEC is the main cause of?

A

Traveller’s diarrhoea

69
Q

ETEC is the leading cause of death in?

A

Children <5 years of age

70
Q

How does ETEC colonise?

A

EtpA

71
Q

What is EtpA?

A

It is an adhesin
Interacts with the tips of ETEC flagella to promote adhesion by forming molecular bridges between the bacteria and the epithelial surface

72
Q

What toxins does ETEC secrete?

A

ST and LT toxins

73
Q

ST toxin?

A

Heat Stable Toxin

74
Q

LT toxins?

A

Heat Labile Toxin

75
Q

Which is larger ST or LT?

A

Lt is larger than ST

76
Q

Which toxin is very similar to the cholera toxin?

A

LT

Heat Labile toxin

77
Q

Structure of the heat labile LT toxin?

A

A subunit and 5 identical B subunits

78
Q

What receptor does LT bind to?

A

GM1 receptor- same receptor that the cholera toxin binds to

79
Q

What is GM1?

A

Ganglioside receptor

80
Q

What does the B subunit of LT do?

A

Binds to the GM1 ganglioside receptor

81
Q

What does the A subunit of LT do?

A

Has the biological enzymatic activity

82
Q

LT remains associated with outer membrane vesicles via?

A

Interactions with LPS

83
Q

What is a proposed reason for ETEC being a milder disease than cholera?

A

Lots of cholera toxin can be secreted. However, ETEC LT is associated with outer membrane vesicles due to interactions with LPS, so smaller amounts reach host cells

84
Q

How does LT cause disease?

A

Associated with outer membrane vesicles
Comes into contact with GM1 ganglioside receptor
B subunit binds GM1 and the vesicle is endocytosed
A subunit can lead to cAMP activation
CFTR is phosphorylated and activated
Cl- ions move into the lumen of the intestines. Followed by Na+ and water.
High levels of water cause watery diarrhoea

85
Q

How does ST cause disease?

A

Binds to guanylyl cyclase C (GC-C) on the intestinal epithelium
Activates the intracellular domain of guanylyl cylase
Leads to intracellular accumulation of cGMP
Activates cGMP-dependent protein kinase II
Phosphorylation of CFTR
Cl- secretion

86
Q

ST binds and activates?

A

Guanylyl cylase C (GC-C)

87
Q

LT binds?

A

GM1 ganglioside

88
Q

What are the T3SS dependent pathogenic E.coli?

A

EIEC
EHEC
EPEC

89
Q

What are the main differences between EHEC and EPEC?

A

EHEC has a natural reservoir in cattle

EHEC can produce Shiga toxin

90
Q

As EHEC produces shiga toxin it can be known as?

A

STEC

Shiga toxin producing E.coli

91
Q

EPEC colonises?

A

The small intestine

92
Q

EHEC colonises?

A

The large intestine

93
Q

What is the main symptom of EHEC infection?

A

Bloody diarrhoea

94
Q

Which serotype of EHEC causes lots of infections due to infected lettuce and food?

A

O157:H7

95
Q

The T3SS of EPEC and EHEC is encoded by?

A

LEE

Locus of enterocyte effacement

96
Q

What does LEE stand for?

A

Locus of enterocyte effacement

97
Q

What is LEE, the locus of enterocyte effacement?

A

It is a 35.6 kb pathogenicity island

98
Q

What does LEE encode?

A

Encodes the T3SS as well as effectors such as adhesin intimin and Tir

99
Q

How was the LEE pathogenicity island obtained?

A

Through horizontal gene transfer

100
Q

What can the T3SS be described as?

A

A molecular syringe

101
Q

Describe the T3SS structure?

A

Have rings which provide a continuous path between the inner and outer membranes. Attached to the outer-membrane ring is a needle. The needle capped and extended by a filamentous extension (EspA). EspB and EspD assemble at the tip of EspA and insert into the host membrane to form a pore.

102
Q

What extends the needle of the T3SS in EPEC and EHEC?

A

EspA filamentous extension

103
Q

What is found at the tip of the EspA filamentous extension?

A

EspB and EspD

104
Q

What does the EspA filamentous extension allow?

A

EspA is thought to facilitate attachment to the host cells through the thick glycocalyx layer

105
Q

Shigella T3SS lacks?

A

EspA filamentous extension

106
Q

As Shigella T3SS lacks EspA it cannot?

A

Shigella lacks the additional extension which means it cannot facilitate attachment to host cell through the thick glycocalyx layer.

107
Q

What are some T3SS effectors in EHEC/EPEC?

A 
Tir
Adhesin intimin
EspH
EspM
EspT
Nlec
108
Q

Tir and intimin allow for?

A

Intimate adherence

109
Q

What forms as a result of EPEC/EHEC intimate adherence?

A

A/E lesions

110
Q

How is intimate adherence established?

A

Tir enters host cells via T3SS and embeds into the host cell membrane- hairpin loop extends extracellularly
Intimin is expressed on the bacterial cell surface and binds Tir

111
Q

What happens once Tir and intimin bind?

A

Formation of actin rich pedestals

N-WASP is activated and can tripper Arp2/3 actin polymerisation

112
Q

What are A/E lesions?

A

Formed as a result of intimate adhesion
Characterised by intimate binding, destruction of the brush border microvilli and accumulation of polymerised actin to form a pedestal structure.

113
Q

When are Rho GTPases active?

A

When bound to GTP

114
Q

When are Rho GTPases inactive?

A

When bound to GDP

115
Q

What are Rho GTPases?

A

Family of G proteins

116
Q

Rho GTPases have a function in?

A

Regulating intracellular actin dynamics

117
Q

How are Rho GTPases activated/ when can signalling occur?

A

When Rho GTPases are bound to GTP

Can be activated by GEFs which exchange GDP for GTP allowing signalling to occur

118
Q

How are Rho GTPases inactivated/how can signalling be terminated?

A

Can stimulate the GTPase activity of Rho GTPases causing GTP–>GDP. This terminates signalling.

119
Q

How can EspH impact Rho GTPase signalling?

A

Directly prevents GEFs binding to Rho and prevents Rho activation.

120
Q

How can EspM and EspT impact Rho GTPase signalling?

A

Can activate Rho through molecular mimicry

121
Q

What is the overall purpose of EspH, EspM and EspT?

A

Shuts down the host’s ability to control signalling through Rho and has it’s own way of controlling Rho GTPase signalling

122
Q

What does NleC do?

A

It is a protease and is able to cleave the p65 subunit of NF-kB to inhibit TLR signalling

123
Q

Shiga toxin structure?

A

5 B subunits

1 A subunit

124
Q

B subunit of shiga toxin binds?

A

Gb3

125
Q

A subunit of shiga toxin does what?

A

Can cleave the 28S rRNA of the 60S ribosome which disrupts protein synthesis and induces apoptosis

126
Q

Why are cattle not impacted by shiga toxin?

A

Endothelial cells of cattle do not express Gb3 which prevents shiga toxin binding blood vessels in the gastrointestinal tract of cattle.

127
Q

Why should EHEC not be treated with antibiotics?

A

Shiga toxin is encoded by a phage. Shiga toxin is produced during the lytic stage of the phage cycle. Antibitoics can induce stress which causes the phage to enter the lytic cycle= even more shiga toxin produced.

128
Q

Why should EHEC not be treated with antibiotics?

A

Shiga toxin is encoded by a phage. Shiga toxin is produced during the lytic stage of the phage cycle. Antibiotics can induce stress which causes the phage to enter the lytic cycle= even more shiga toxin produced.

129
Q

ETEC infects the?

A

Small intestine

130
Q

EAEC infects the?

A

Ileum of the small intestine/ large intestine

131
Q

EHEC infects the?

A

Large intestine

132
Q

Shigella infects the?

A

Large intestine

133
Q

EPEC infects the?

A

Small intestine

MM- Bacteria (7 decks)

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