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HHAD: Microbiology > Pathogenicity: Virulence and determinants > Flashcards

Pathogenicity: Virulence and determinants Flashcards

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Biology 101 flashcards
1
Q

What are the features of endotoxins LPS (lipopolysaccharide)? (5)

A
  • Produced by gram negative bacteria
  • Heat stable and poorly antigenic (hard to kill - even using autoclave)
  • Shock, fever, 50,000 deaths in USA
  • Lipid A associates with LPS binding protein (LBP) and binds to receptor CD14 in conjunction with TLR4
  • Triggers signalling: cytokine release (cytokine storm), iNOS activation, inflammation
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2
Q

What molecule does LPS bind with to form a complex?

A

LBP (LPS binding protein)

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3
Q

Which receptors recognise LPS?

A

TLR4/CD14/MD2 receptor complex

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4
Q

What happens when the receptor complex (on macrophages and monocytes) has recognised LPS?

A

Activates mass production of pro-inflammatory cytokines

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5
Q

What is endotoxaemia?

A

The presence of LPS in the bloodstream which leads to cytokine storn

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6
Q

In what illness/disease is LPS a main driving agent?

A

Sepsis and septic shock

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7
Q

What are the 2 different types of exotoxins?

A

Membrane-acting toxins

Intracellular toxins

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8
Q

What are the actions of membrane-acting toxins?

A
  • Enzymatic: lead to digestion/break down constituents of membrane
  • Pore formation: form pores through membrane
  • Perturbs signalling
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9
Q

Which is the most notable enzyme involved in exotoxin activity?

A

Phospholipase (C. albicans can produce this)

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10
Q

Which organism can produce pore formation?

A

E Coli alpha-haemolysin

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11
Q

What toxin is produced by enterotoxigenic E Coli (ETEC)?

A

ST Toxin

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12
Q

How does the ST toxin work?

A

It works by binding to the extracellular domain pf guanylylcyclase C
- molecular mimicry (similar to natural ligand guanylin).

This then activates the intracellular catalytic domain to produce cGMP.

Higher levels of cGMP then leads to exflux of Cl- and prevents influx of Na+, leading to osmotic diarrhoea.

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13
Q

What superantigen derives from S Aureus?

A

TSST-1

this causes Toxic shock syndrome due to excessive activation of T cell immune response

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14
Q

How do super antigens work?

A

They associate with the MHC class 2 receptor on antigen-presenting cell, they then cross-link this with generic V (variable)- Beta region on Y cell receptors from non-specific T cell.

This is a non-specific t cell activation

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15
Q

How are intracellular toxins classified?

A

Classified by enzymatic activity now

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16
Q

What are the 3 main attributes of intracellular toxins?

A

Bind to cell surface
Cross the membrane to gain entry
Enzymatic activity

17
Q

How do intracellular toxins attack cells?

A
  1. Cell binding
  2. Membrane translocation
  3. Enzymatic activity
18
Q

What 2 subunits make up AB toxins?

A

A fragment - active

B fragment - binding

19
Q

Give 3 examples of AB toxins

A

diphtheria
tetanus
botulinum

20
Q

What is an example of an A2B toxin (so 2 active subunits and 1 B subunit)?

A

Anthrax

21
Q

Name 2 neurotoxins

A

Botulinum

Tetanus

22
Q

How do neurotoxins work?

A

They attack signalling between nerve cells.

They do this by preventing fusion of the vesicles containing the neurotransmitters

23
Q

Which enzyme do we tend to see associated with neurotoxins?

A

Zinc proteases

24
Q

How does tetanus toxin work?

A

It works by preventing the release of the inhibitory transmitters, so the signal is never turned off so it is long and drawn out

25
Q

How does botulinum toxin work?

A

Prevent excitory transmitter vesicles from fusing with synaptic membrane, so signal is never actually instigated

26
Q

What are the symptoms associated with tetanus toxin? (4)

A

restlessness
headaches
irritability
Muscle spasms (Lockjaw)

27
Q

What symptoms are most associated with botulinum? (4)

A

Muscle weakness
Excess sweating
dry mouth
Parkinsons

28
Q

What are the symptoms of diphtheria?

A

Inflamed throat, diphtheric membrane in throat, fever

29
Q

How is diphtheria treated?

A

Antitoxin, antibiotics, rest

30
Q

What is the mechanism of action for diphtheria?

A

It prevents the elongation of EF-2 (elongation factor 2).
EF-2 is major component of protein-synthesis pathway
ADPribose (ADP ribosolase enzyme) - which inactivates EF2 and prevent elongation of protein

31
Q

How does toxin translocation work in a diphtheria molecule?

A

alpha helices in transmembrane domain contain negatively charged loops between each helices.
The conditions become acidic when it is taken up.
This negative charge attracts hydrogen ions.
This allows the helices to closely associate with the membrane and they can pass through.

32
Q

What are the modes of action of ADP-ribosylating toxins and examples of these?

A

Modifies EF2 (ie blocks protein synthesis): e.g. diphtheria toxin

Modify signalling proteins e.g. cholera, E Coli LT

33
Q

Give 3 examples of non-toxin diseases

A

Plague - yersinia pestis
Typhoid - salmonella typhi
Shigellosis(intestinal infection - main sign diarrhoea) - shigella flexneri

34
Q

What system is the most notable type of injection into the cell?

A

Type 3/4 secretion systems

35
Q

From what has the type 3 secretion system evolved?

A

Flagellum

36
Q

From what has the type 4 secretion system evolved?

A

Pili

37
Q

How does the type 3 secretion in Yersinia work?

A

The protein complex spans the inner and outer membrane and is compressed. When it comes into contact with the eukaryotic cell membrane, it decompresses and protrudes into target cell. it then secretes different toxins and enzymes through this pore into target cell.

38
Q

Which is a newer type of secretion system that has been discovered and from what has this evolved?

A

Type 6
evolved from bacteriophages
e.g. vibrio cholera

39
Q

Why are toxins so potent?

A

Their target choice - they often target key cellular components (e.g. membrane, protein synthesis, signalling mechanisms).
Enzymatic action - usually means even one molecule can kill a cell

HHAD: Microbiology (6 decks)

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