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Shigella Flashcards

(96 cards)

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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
What mechanism allows Shigella to overcome colonisation resistance of commensals?
Can produce colicins which are antimicrobial peptides. These colicins can kill the commensal bacteria and reduce competition
26
What are colicins?
They are antimicrobial peptides
27
What is LPS?
Lipopolysaccharide | Endotoxin
28
LPS structure?
O antigen Core region Lipid A
29
What is the O antigen?
The O antigen is made up of repeats of an oligosaccharide unit
30
How does the O antigen exhibit variation?
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.
31
The O antigen for Shigella sonnei is?
Structurally unique
32
Shigella sonnei has an O antigen almost identical to those present in?
Plesiomonas shigelloides chromosome
33
O antigen for Plesiomonas shigelloides is encoded on?
A chromosome
34
The O antigen for Shigella sonnei is encoded on
A plasmid
35
Why the O antigen of S.sonnei located on a plasmid?
Inactivated the O antigen encoded on the chromosome and acquired a new coding region for the O antigen on a plasmid
36
How many serotypes of S.sonnei are there?
A single serotype
37
What is different about the O antigen of S.sonnei?
It is much simpler and shorter
38
Immunity to S.sonnei in communities with contaminated water supplies?
Many have been provided by Plesiomonas shigelloides infection.
39
It is thought that Shigella evolved from?
Non-pathogenic E.coli
40
How did Shigella evolve from non-pathogenic E.coli?
- Gain of a virulence plasmid - Gain of pathogenicity islands - Loss of 'antivirulence' genes such as ompT and cadA
41
What is the virulence plasmid?
Encodes virulence effectors | Also encodes the T3SS
42
Shigella encodes virulence factors on?
The virulence plasmid and chromosomally
43
What toxin is encoded chromosomally?
ShET1
44
ShET1 is encoded on?
Pathogenicity island on the chromosome
45
What are the pathogenicity islands in Shigella known as?
Shigella pathogenicity islands= SHIs
46
What pathogenicity island encodes ShET1 enterotoxin?
SHI-1
47
What are two "anti-virulence" genes that have been lost?
ompT and cadA
48
How does OmpT impede virulence?
OmpT inhibits the spread of Shigella by interfering with the polar localisation of the actin nucleator protein IcsA
49
What is OmpT?
An outermembrane protease
50
What is IcsA?
IcsA is an actin nucleator protein
51
What is the function of IcsA?
It is an actin nucleator protein and is needed for actin polymerisation
52
IcsA recruits?
Recruits N-WASP which then leads to the recruitment of Arp2/3
53
What does Shigella use actin polymerisation for?
Uses it for cell-to-cell spread
54
What does cadA gene encode?
Encodes a lysine decarboxylase
55
What does lysine decarboxylase (encoded by cadA) do?
Catalyses the production of polyamine cadaverine
56
What does polyamine cadaverine do?
Inhibits the function of Shigella enterotoxins which lessens the disease
57
cadA encodes?
Lysine decarboxylase
58
What does lysine decarboxylase do?
It leads to the production of polyamine cadaverine
59
Polyamine cadaverine does what?
It inhibits the function of Shigella enterotoxins
60
Why was Shigella motility lost?
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
Shigella infects which cells primarily?
M cells
62
What are M cells?
Microfold cells | Part of the specialised epithelium
63
What do M cells do?
They continuously sample antigen from the gut lumen and transcytose it to the basal cell membrane
64
Why does Shigella infect M cells?
Needs to reach the basal side of the epithelium so it can infect epithelial cells
65
Why can't Shigella infect epithelial cells directly?
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
M cells do not have?
They do not have microvilli on their surface | They do not have a thick glycocalyx
67
How does Shigella reach the epithelial cells?
Reaches the epithelial cells via the filopodia
68
What are filopodia?
Cell surface sensory organelles
69
What does the eukaryotic cell use filopodia for?
Sensing, migration and cell-cell interaction
70
What does Shigella use the filopodia for?
Shigella establishes contact with the filopodia-like extensions, which retract to bring bacteria in contact with the cell body where invasion occurs
71
Once the Shigella has been transcytosed it is?
Taken to the basal cell membrane, where lots of macrophages are present. May be phagocytosed by the macrophages.
72
How does Shigella enter cells, including M cells?
Membrane ruffling
73
How do the bacteria escape the macrophages?
By inducing apoptosis
74
Once released from the dying macrophage what does the Shigella do?
Enters epithelial cells via the basolateral side
75
How does Shigella enter epithelial cells?
Through membrane ruffling
76
How does Shigella cause membrane ruffling?
T3SS | Injection of T3SS effectors which reorganise the actin cytoskeleton and leading to the formation of membrane ruffles
77
How can Shigella move around the cell and to other cells if it is non-motile?
By utilising host cell actin polymerisation
78
What is needed for actin polymerisation and movement of Shigella?
IcsA
79
What is IcsA?
An outer membrane protein
80
Where is IcsA localised?
Polarly
81
How does actin polymerisation occur?
Polar localisation of IcsA outer membrane protein.
82
What does IcsA do?
IcsA protein promotes actin nucleation | Recruits N-WASP
83
N-WASP recruits?
Actin polymerisation Arp2/3 complex
84
Actin polymerisation process?
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
Shiga toxin is associated with which shigella species?
S.dysenteriae
86
Shiga toxin is also produced by E.coli known as?
STEC- shiga toxin producing E.coli
87
STEC can produce which shiga toxins
Stx1 or Stx2
88
Which STEC shiga toxin is identical to that produced by Shigella?
Stx1
89
Shiga toxin structure?
1 A subunit and 5 B subunits | AB5 structur
90
Shiga toxin binds to which receptor?
Gb3
91
B subunit binds to?
Gb3 receptor
92
What does the A subunit do?
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
28S rRNA is part of?
The 60S ribosomal subunit
94
The shiga toxin of S.dysenteriae is produced by?
A dysfunctional/defective prophage
95
As the phage of S.dysenteriae is defective?
You can treat infection with antibiotics without worrying that more Shiga toxin will be produced. Cannot enter the lytic cycle.
96
Can you treat EHEC with antibiotics?
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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