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MM- Bacteria > Shigella > Flashcards

Shigella Flashcards

1
Q

Is Shigella motile?

A

No

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2
Q

Shigella has the same life cycle as?

A

EIEC- Enteroinvasive E.coli

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3
Q

How to differentiate Shigella from E.coli?

A

Shigella tends to be a lactose non-fermenter
Shigella does not produce gas when breaking down carbohydrates e.g. glucose fermentation
Shigella is non-motile - has no flagella= H antigen or fimbriae

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4
Q

Shigella classification?

A

Family: Enterobacteriaceae
Genus: Shigella

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5
Q

Shigella causes?

A

Shigellosis

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6
Q

Symptoms of Shigella infection?

A

Diarrhoea which is often bloody

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7
Q

Serious complications of Shigella infection?

A

Encephalopathy- brain infection
HUS- Hemolytic uremic syndrome
Convulsions

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8
Q

What is HUS?

A

Hemolytic uremic syndrome

It is the loss of platelets, a low red blood cell count (anaemia) and kidney failure

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9
Q

What Shigella infection can cause HUS?

A

Shigella dysenteriae

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10
Q

How many known species of Shigella are there?

A

Four

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11
Q

What are the four Shigella species?

A

Shigella boydii
Shigella flexneri
Shigella sonnei
Shigella dysenteriae

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12
Q

How many serotypes of Shigella sonnei are there?

A

Only a single serotype

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13
Q

S.flexneri is usually found where?

A

Most common in low/middle income countries

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14
Q

S.sonnei is usually found where?

A

Developed/industrialised countries

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15
Q

S.dysenteriae is usually found where?

A

Sporadic infection

Usually associated with outbreaks

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16
Q

Rates of S.sonnei increase with?

A

Increased economic development

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17
Q

How is Shigella transmitted?

A

Fecal-oral route

Poor sanitation

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18
Q

As a country becomes richer?

A

Increase in rates of S.sonnei and a decrease in the number of S.flexneri infections

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19
Q

Main differences between Shigella and EIEC?

A

Shigella does not produce gas as it breaks down carbohydrates
Shigella spp. tend to be lactose fermenters
Shigella is non-motile, lacks flagella and fimbriae

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20
Q

How can Shigella be transmitted?

A 
Fecal-oral route
Poor toilet behaviour
Contaminated water
Flies breeding on faeces can spread the disease
Poor sanitation
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21
Q

How infectious is Shigella and propose why?

A

Very infectious
Infectious dose can range from 10-100 particles
Thought to be highly infectious as it can resist the acidic pH of the stomach

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22
Q

What factors of Shigella contribute to diarrhoea?

A

Shigella dysenteriae: Shiga toxin

The ShET1 and ShET2 enterotoxins

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23
Q

Where does Shigella establish infection?

A

In the large intestine

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24
Q

Why is Shigella not a good coloniser?

A

Lacks fimbriae

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25
Q

What mechanism allows Shigella to overcome colonisation resistance of commensals?

A

Can produce colicins which are antimicrobial peptides. These colicins can kill the commensal bacteria and reduce competition

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26
Q

What are colicins?

A

They are antimicrobial peptides

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27
Q

What is LPS?

A

Lipopolysaccharide

Endotoxin

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28
Q

LPS structure?

A

O antigen
Core region
Lipid A

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29
Q

What is the O antigen?

A

The O antigen is made up of repeats of an oligosaccharide unit

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30
Q

How does the O antigen exhibit variation?

A

The O antigen exhibits variation in the types of sugar present, their arrangement within the O unit and the linkages within and between O units, making lipopolysaccharide one of the most variable cell constituents.

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31
Q

The O antigen for Shigella sonnei is?

A

Structurally unique

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32
Q

Shigella sonnei has an O antigen almost identical to those present in?

A

Plesiomonas shigelloides chromosome

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33
Q

O antigen for Plesiomonas shigelloides is encoded on?

A

A chromosome

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34
Q

The O antigen for Shigella sonnei is encoded on

A

A plasmid

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35
Q

Why the O antigen of S.sonnei located on a plasmid?

A

Inactivated the O antigen encoded on the chromosome and acquired a new coding region for the O antigen on a plasmid

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36
Q

How many serotypes of S.sonnei are there?

A

A single serotype

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37
Q

What is different about the O antigen of S.sonnei?

A

It is much simpler and shorter

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38
Q

Immunity to S.sonnei in communities with contaminated water supplies?

A

Many have been provided by Plesiomonas shigelloides infection.

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39
Q

It is thought that Shigella evolved from?

A

Non-pathogenic E.coli

40
Q

How did Shigella evolve from non-pathogenic E.coli?

A
  • Gain of a virulence plasmid
  • Gain of pathogenicity islands
  • Loss of ‘antivirulence’ genes such as ompT and cadA
41
Q

What is the virulence plasmid?

A

Encodes virulence effectors

Also encodes the T3SS

42
Q

Shigella encodes virulence factors on?

A

The virulence plasmid and chromosomally

43
Q

What toxin is encoded chromosomally?

A

ShET1

44
Q

ShET1 is encoded on?

A

Pathogenicity island on the chromosome

45
Q

What are the pathogenicity islands in Shigella known as?

A

Shigella pathogenicity islands= SHIs

46
Q

What pathogenicity island encodes ShET1 enterotoxin?

A

SHI-1

47
Q

What are two “anti-virulence” genes that have been lost?

A

ompT and cadA

48
Q

How does OmpT impede virulence?

A

OmpT inhibits the spread of Shigella by interfering with the polar localisation of the actin nucleator protein IcsA

49
Q

What is OmpT?

A

An outermembrane protease

50
Q

What is IcsA?

A

IcsA is an actin nucleator protein

51
Q

What is the function of IcsA?

A

It is an actin nucleator protein and is needed for actin polymerisation

52
Q

IcsA recruits?

A

Recruits N-WASP which then leads to the recruitment of Arp2/3

53
Q

What does Shigella use actin polymerisation for?

A

Uses it for cell-to-cell spread

54
Q

What does cadA gene encode?

A

Encodes a lysine decarboxylase

55
Q

What does lysine decarboxylase (encoded by cadA) do?

A

Catalyses the production of polyamine cadaverine

56
Q

What does polyamine cadaverine do?

A

Inhibits the function of Shigella enterotoxins which lessens the disease

57
Q

cadA encodes?

A

Lysine decarboxylase

58
Q

What does lysine decarboxylase do?

A

It leads to the production of polyamine cadaverine

59
Q

Polyamine cadaverine does what?

A

It inhibits the function of Shigella enterotoxins

60
Q

Why was Shigella motility lost?

A

Uncertain
Thought it is because it is not needed for intracellular infection as actin polymerisation is used for cell-to-cell movement
Thought to allow Shigella to evade immune detection e.g. TLR5 recognises bacterial flagellin

61
Q

Shigella infects which cells primarily?

A

M cells

62
Q

What are M cells?

A

Microfold cells

Part of the specialised epithelium

63
Q

What do M cells do?

A

They continuously sample antigen from the gut lumen and transcytose it to the basal cell membrane

64
Q

Why does Shigella infect M cells?

A

Needs to reach the basal side of the epithelium so it can infect epithelial cells

65
Q

Why can’t Shigella infect epithelial cells directly?

A

Due to the microvilli and thick glycocalyx
The T3SS of Shigella lacks the EspA extension filament of the needle. In EPEC/EHEC the needle of the T3SS is capped by an extension EspA filament which allows penetration through the glycocalyx and into the epithelial cell.

66
Q

M cells do not have?

A

They do not have microvilli on their surface

They do not have a thick glycocalyx

67
Q

How does Shigella reach the epithelial cells?

A

Reaches the epithelial cells via the filopodia

68
Q

What are filopodia?

A

Cell surface sensory organelles

69
Q

What does the eukaryotic cell use filopodia for?

A

Sensing, migration and cell-cell interaction

70
Q

What does Shigella use the filopodia for?

A

Shigella establishes contact with the filopodia-like extensions, which retract to bring bacteria in contact with the cell body where invasion occurs

71
Q

Once the Shigella has been transcytosed it is?

A

Taken to the basal cell membrane, where lots of macrophages are present. May be phagocytosed by the macrophages.

72
Q

How does Shigella enter cells, including M cells?

A

Membrane ruffling

73
Q

How do the bacteria escape the macrophages?

A

By inducing apoptosis

74
Q

Once released from the dying macrophage what does the Shigella do?

A

Enters epithelial cells via the basolateral side

75
Q

How does Shigella enter epithelial cells?

A

Through membrane ruffling

76
Q

How does Shigella cause membrane ruffling?

A

T3SS

Injection of T3SS effectors which reorganise the actin cytoskeleton and leading to the formation of membrane ruffles

77
Q

How can Shigella move around the cell and to other cells if it is non-motile?

A

By utilising host cell actin polymerisation

78
Q

What is needed for actin polymerisation and movement of Shigella?

A

IcsA

79
Q

What is IcsA?

A

An outer membrane protein

80
Q

Where is IcsA localised?

A

Polarly

81
Q

How does actin polymerisation occur?

A

Polar localisation of IcsA outer membrane protein.

82
Q

What does IcsA do?

A

IcsA protein promotes actin nucleation

Recruits N-WASP

83
Q

N-WASP recruits?

A

Actin polymerisation Arp2/3 complex

84
Q

Actin polymerisation process?

A

IcsA is an outer membrane protein of Shigella
It has polar localisation
N-WASP is recruited
Arp2/3 complex is recruited which results in actin nucleation

85
Q

Shiga toxin is associated with which shigella species?

A

S.dysenteriae

86
Q

Shiga toxin is also produced by E.coli known as?

A

STEC- shiga toxin producing E.coli

87
Q

STEC can produce which shiga toxins

A

Stx1 or Stx2

88
Q

Which STEC shiga toxin is identical to that produced by Shigella?

A

Stx1

89
Q

Shiga toxin structure?

A

1 A subunit and 5 B subunits

AB5 structur

90
Q

Shiga toxin binds to which receptor?

A

Gb3

91
Q

B subunit binds to?

A

Gb3 receptor

92
Q

What does the A subunit do?

A

The A subunit removes an adenine residue from 28S rRNA which is part of the 60S ribosomal subunit. Prevents protein synthesis from occurring which induces apoptosis

93
Q

28S rRNA is part of?

A

The 60S ribosomal subunit

94
Q

The shiga toxin of S.dysenteriae is produced by?

A

A dysfunctional/defective prophage

95
Q

As the phage of S.dysenteriae is defective?

A

You can treat infection with antibiotics without worrying that more Shiga toxin will be produced. Cannot enter the lytic cycle.

96
Q

Can you treat EHEC with antibiotics?

A

No as the prophage encoding Stx will enter the lytic cycle as the antibiotics induce stress in the bacterial cells they occupy

MM- Bacteria (7 decks)

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