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Molecular Microbiology > Virulence Factors in detail > Flashcards

Virulence Factors in detail Flashcards

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Biology 101 flashcards
1
Q

What are the two ways a bacteria can attach?

A

1) pili (fimbriae): usually the tip of the pili

2) adhesions

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2
Q

What is the difference between adhesions and pili?

A

Pili are long with many subunit but adhesions are short and have one or two subunits

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3
Q

How does the human body usually expel invaders

A
  • shed dead skin
  • urine from bladder at high speed
  • coughing
  • cilia in lungs constantly moves mucus up
  • peristalsis in intestines to move contents
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4
Q

What are gram positive pili like?

A

all the different pilin subunits are covalently joined together and pilus is covalently joined to the cell wall.

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5
Q

What are two main types of pili in gram negative bacteria?

A
  • Type 1: adheres to mannose

- Type 4:

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6
Q

Describe type 1 pili

A

They anchored to outer membrane and they cannot be retracted; they are not static.
At the end of pilus there is a specialised lectin which can bind to sugars; type 1 binds to mannose

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7
Q

Describe type 4 pili

A

-They are anchored to the inner membrane and can be retracted; they are static
-The pilus is made by polymerising together lots of monomers of pilin proteins to make a long fiber.
-Upon retraction, pilin in fiber depolymerises from the bottom to make shorter fiber
-external terminal of pili adheres via tip to host cells where retraction can draw bacteria closer to cell
“like a grappling hook”

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8
Q

Where are the genes of making pilus found?

A

The operon; many pilus operons are regulaed/ expressed under infection conditions.
This means the amount of pilin/other proteins made is controlled at different stages of infection

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9
Q

What is an operon?

A

group of genes that are expressed from the same promoter; this means genes can be regulated at he same time

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10
Q

Describe the strucure of an operon gene containing pilus genes

A

regulation region beore promoter. First major pilus gene segment (pilA) which is needed to make pilus subunit. This is transcribed in excess, more than other protein.
Other proteins on the operon are rod terminator, outer membrane usher, periplasmic chaperone, adaptor, major tip component, mannose binding adhesion

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11
Q

How is Type 1 pili made in Uropathogenic E.coli?

A

protein components made in cytoplasm get out of inner membrane, across periplasm to outer membrane where they are assembled on outer surface of this membrane.

They are transported by Sec machinery; there is a membrane channel that drives transport

PapD is between the membranes protein secreted via Sec is chaperoned to outer membrane by PapD.

PapC channel is on the outer membrane which subunits go through and accumulate on the outer side

PapG protein binds to host cell membrane

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12
Q

What is the Sec system? What are the subunits/machinery involved?

A

required for the export of almost all external proteins.
SecY (protein)
SecA (ATPase): hydrolysis of ATP transports the protein across membrane.
SecB is a chaperone: binds to newly synthesised proteins and stops them from folding so they can be transported.

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13
Q

What are the properties of the Sec channel, what does this mean?

A

The channel is very narrow and so can only transport unfolded proteins. SecB chaperone prevents folding

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14
Q

How is Type 4 pili made in V.cholerae?

A

This type can both grow and retract and so needs assembly and disassembly.
Major pilus subunit formed from PilA protein made inside the cell and exported across the membrane: channel SecY doesnt need Sec-A instead it needs signal recognition particle (SRP)

pilA pushed through channel by the ribosome and escapes through the Sec channel in the inner membrane.

PilD processes the pilA protein as it removes first 5 aa.

Processed protein assembled/polmerised into a fiber by PilF (Atpase) where monomers form complexes in periplasm (space between membranes); there are no free pilA subunits.

PilQ needed for growing pilus to cross outer membrane.

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15
Q

What is SRP

A

SRP grabs pilA protein whilst is it still being translated on the ribosome and guides it to the sec channel on the inner membrane.

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16
Q

What is the essential step in Type 4 pili assembly/

A

PilD proceesing; 5 aa removed so pilus can assemble

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17
Q

Describe pilF

A

It is an ATPase which uses the energy from ATP hydrolysis to push pilA protein out of the membrane.

Hydrophobic patch on pilA that interacts with the membrane that also binds tightly to another pilA monomer, forming a complex once it exits the membrane

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18
Q

What is PilQ?

A

A large hole in the middle and it allows the growing pilus to pass through it.

Without this gene the pilus cant get out of the cell and it forms a massive structure in the periplasm and cell dies.

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19
Q

Describe type 4 retraction of pili

A

needs action of pilT (ATPase)

It is unknown what causes this, and unknown the fate of pilA subunits

20
Q

Describe adhesions

A

one type of protein that may form dimers or trimers with itself.
Adhesions attached to surface of bacteria, sticking out a little.

21
Q

Give examples of an adhesion

A
  • M protein fibrils seen on Streptococcus which bind to fibronectin and complement Factor H
  • lollipops sructures of YadA adhesion of Yersinia bacteria which binds to collagen
22
Q

What are the two types of toxins?

A

1) Exotoxin: secreted by the cell

2) Endotoxin: only in gram negative and part of the outer membrane as part of their overall makeup.

23
Q

Describe the asymmetric nature of bacterial outer membranes. What is LPS

A

inner leaflet is made up of phospholipids but the outer leaflet is made of LipidA. Lipid A is modified with sugar side chains. These sugars define different strains of bacteria.
LipidA and sugar complexes are called lipopolysaccharide (LPS) where the lipid A is toxic.

24
Q

How do gram negative outer membranes cause toxic effects?

A

Lipid A part of LPS is usually hidden behind sugar, it is released when bacteria dies and leads to an inflammatory response or toxic shock.

25
Q

Describe exotoxins

A

The are made specifically to attack host processes inside cell with different categories of different categories

26
Q

What are the five categories of exotoxin action?

A
  • Membrane distruption
  • Distruption of protein synthesis
  • Second messenger pathway disruption/interfering with signalling
  • Superantigenic toxins
  • Proteases that cleave host components
27
Q

What is a superantigen?

A

not processed normally by T cells, instead they activate straight away to cause autoimmune response and to many activated T cells.

For example, pyrogenic toxin of Staph aureus causing toxic shock syndrome

28
Q

Exotoxin: membrane disruption. How does alpha toxin work?

A

The toxin haemolytic alpha toxin of staph aureus. Here, alpha toxin is a single polypeptide chain which causes respiratory paralysis, vascular and smooth muscles spasms, cytolysis.

alpha toxin monomers bind the cell membrane and form a heptamer which makes a beta barrel in the host cell membrane.
protein hydrophobic residues point outwards into the membrane; hydrophilic residues point inward on the interior of the channel which form the pore.

ions, ATP, NADH, glutathione will be lost through pore. Water flows in and lyses the cell.

40% of toxins disrupt plasma membranes

29
Q

Exotoxin: disruption of protein synthesis. How does Shiga toxin work?

A

many targets of ribosomes (protein,RNA subunits) and translation (elongation factors and tRNA)
Shiga requires specific receptors on cells surface so it can attach and enter the cell.

When inside A subunit functions as a N-glycosidase which cleaves adenine nucleobase from 28SRNA of 60S subunit of ribosome.

Therefore stops translation and the cell dies as endothelium cannot renew itself.

30
Q

What is the specific receptor for Shiga toxin of E.coli/Shigella

A

ganglioside Gb3; species such as cattle,swine, deer have these receptors.
Animal feces spreads bacteria to humans

31
Q

Describe the structure of the Shiga toxin

A

MW: 68000da; it has many subunits containing one A subunit and five B subunits. A subunit is needed for the toxic action of the protein. B subunit is needed for binding to specific cells and uptake by endocytosis.

32
Q

What are AB toxins

A

Like Shiga, there is an A subunit and a B subunit: the A subunit is the ACTIVE component which mediates toxicity
B subunit is the BINDING component which guides toxin to target cell and pore entry.

33
Q

What is an example of an A subunit of the AB toxins?

A

Most are ADP-ribosyltransferase enzymes like cholera toxin.

These enzymes cleave NAD and use ADP-ribose to stick onto a target protein.

The toxin is specific; cholera and diptheria toxin both ADP ribosylate a protein but the target is different

34
Q

What are he two ways the B subunit of a AB toxin works?

A

1) DIRECT entry: the B subunit bind to specific receptor and induces formation of a pore in the membrane for A transfer
2) Receptor-mediated endocytosis (RME) where the toxin is internalized by the cell in a vesicle called an endosome. H+ ions enter endosome which lowers the pH and thus separates A and B subunits. Now the B allows the A to be released so it can get to target within the cytoplasm. B remains in endosome and is recycled to cell surface.

35
Q

Describe the diptheria toxin

A

It is a rare AB toxin made as a single polypeptide so A and B regions are not separate proteins, they are separate domains.
B binds to cell receptor and protein is internalised. Endocytosis the A and B domains are cleaved but attached via disulphide bonds between cysteine residues.

Endosome acidifies to pH5 so disulphide bonds are reduced and fragments separate.

A is released with it hydrphobic patch which inserts into endosome membrane and allow A peptide to escape.

A cleaves NAD, and sticks ADP-ribose onto elongation factor EF2. This means no elongation during translation and cell death

36
Q

What are the effects of diptheria toxin/symptoms

A

-organism in pharynx behind the nose but the toxin circulates the body via the blood. It causes the growth of pseudomembrane across the trachea.

This contains fibrin and bacteria and human cells

37
Q

What are examples of second messenger pathway distruption?

A

1) ETEC STABLE toxin
2) Cholera toxin
3) ETEC LABILE toxin

Cholera and lable ETEC have same mode of action that affect second messenger cAMP and alters electrolyte transport.

Stable ETEC affects cGMP

38
Q

Describe ETEC toxin (ST)

A

peptides of 2000daltons; they are small and so not activated by heat. These toxins act EXTERNALLY; they are not taken up by the cells.
STa binds to extracellular ligand binding site of guanylate cyclaseC (GC-C) receptor. Receptor activated causing increase in cGMP inside the cell.

This alters electrolyte transport adversely where CL- goes out but Na+ absorption is stopped. It also water out causing diarrhea.

39
Q

Where is Guanylate cyclase C located in the body?

A

brush border membrane of intestine epithelial cells

40
Q

How does enzyme adenylate cyclase work.

A

This enzyme makes cAMP and is regulated.

When G complex is activated and GTP is now part of complex; the alpha has bound to GTP and now dissociates from receptor still bound to GTP where it interacts with enzyme; G-a-GTP bins adenylate cyclase

Gfactor complexes: Gi and Gs where Gs activates enzyme and Gi inhibits enzyme.

When bond to enzyme alpha hydrolyses GTP back to GDP causing unbinding from enzyme. alpha chain goes back to receptor to stimulate again.

41
Q

Describe GI and GS G factor complexes in the cell

A

Made of three subunits: alpha, beta and gamma subunit. Gi and Gs differ in the alpha subunit.

they sit on the membrane as they are bound to a receptor which binds hormones.

The G complex signals the response to the cell after binding. This leads to conformation change.

Conformational change of receptor means GDP in complex is replaced with a GTP via the alpha subunit.

42
Q

How do cholera and labile ETEC work?

A

Cholera toxin (AB toxin) binds to ganglioside receptor (GM1) on host cells, gets internalised via endocytosis.

toxin in endosome gets moved to gogi. In golgi, alpha subunit is recognised by chaperone in E.R called PROTEIN DISULPHIDE ISOMERASE.

alpha is unfolded from AB complex and taken to membrane via the Sec61 channel but on the way alpha refolds.

Alpha binds to human partner ADP ribosylation factor 6 (Arf6) which changes conformation of alpha so it show active site for catalytic activity.

exposed active site ADP-ribosylates G-alpha protein of G complex. this means the alpha subunit of G complex can activate adenylate cyclase enzyme but there is a defective GTPase.

So GTP is not degraded into GDP as is is supposed o can this means there is too much cAMP production.

increased cAMP, activated human kinase A which activated ion transport channels.

43
Q

What channel is activated by the elevated cAMP levels caused by cholera toxin?

A

CFTR channel whiich controls chloride transport; chloride/sodium/water leave. This causes watery stool and diarrhoea.

44
Q

How doe diarrhoea help he microbe?

A

helps spread/dissmination to new hosts and removes completion within the gut.

45
Q

Alpha chain stops GTP degrading so Camp rises

A

cAMP is the second messenger and Protein kinase is the effector

Molecular Microbiology (4 decks)

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