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BIO 315 > Module 12: Bacterial Pathogenesis ( Endotoxins + AB Toxins) > Flashcards

Module 12: Bacterial Pathogenesis ( Endotoxins + AB Toxins) Flashcards

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1
Q

Toxin

(Give regular definition AND definition for pathogenic bacteria)

A

A poisonous substance produced by an organism

For pathogenix bacteria:
–> Common VFs used by bacteria to gain nutrients from their hosts!

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2
Q

What are the 4 main classes/types of toxins?

A

1) Endotoxins
2) AB Toxins
3) Superantigens
4) Cytotoxins (ctolysins)

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3
Q

Exotoxin

A

Soluble proteins (originating in the bacterial cytoplasm) that are actively secreted to the external environment OR passively released by bacterial lysis

Essentially: Toxins that are RELEASED outside the producing cell!

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4
Q

What are the 3 main groups of exotoxins?

A

1) AB Toxins
2) Cytolysins
3) Superantigens

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5
Q

Endotoxins

A

Substances that are PART OF the cell wall structure (not actively released from the cell while alive!)

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6
Q

What are the endotoxins of Gram (-) and (+) bacteria?

A

Gram (-) = LPS (Lipopolysaccharide)

Gram (+) = LTA (Lipoteichoic Acid)

(+) = retains dye/color = THICK wall, (-) = no color = THIN wall

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7
Q

Cytotoxins

A

Toxins that act DIRECTLY on host cells

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8
Q

Can exotoxins or endotoxins be cytotoxins?

Why?

A

EXOtoxins CAN be cytotoxins BUT ENDOtoxins CANT be cytotoxins

== Some exotoxins leave their bacterial cell to go and DIRECTLY elicit an effect on their target cells

BUT

== Endotoxins (when released) trigger an IMMUNE RESPONSE (inflammation) which is what leads to an effect on the target cells! (they do not directly interact with the target cells)

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9
Q

Many pathogens cause disease strictly by the ______________ they produce

What happens when they CANT produce this element?

A

Strictly by the TOXINS they produce!

When they lost the ability to produce these toxins, the bacteria become NON-PATHOGENIC!

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10
Q

Explain the discovery of the 1st endotoxin

A

Scientists found a heat-stable substance associated with the toxic effects observed due to Gram (-) bacterial infections (1890)

–> Named it “endotoxin” because they thought it originated within the cytoplasm (endo) and released upon lysis

== They were partly wrong; this was later identified as LPS

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11
Q

LPS =

AKA?

A

LPS = Lipopolysaccharide

AKA. “Endotoxin”

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12
Q

What are the main structural components of LPS?

A

1) Lipid A (anchors to the OM)

2) Core Polysaccharide

3) O-Antigen

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13
Q

Lipid A

A

The hydrophobic portion of LPS that anchors the LPS molecule to the OM

AND it is responsible for the toxic properties of LPS (triggering inflammatory response)

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14
Q

Core Polysaccharide

A

A complex of various sugars with side chains == composition is HIGHLY conserved between species and genera

–> Extends into the ECF from the OM

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15
Q

O-Antigen

A

Structure at the TIP of LPS that consists of many repeating polysaccharide units == its composition is highly variable (characteristic of specific species)

–> A major antigenic target of the antibody immune response!

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16
Q

LPS vs LPO

A

LPS = Lipopolysaccharide
(Has Lipid A, Core Polysaccharide, O-antigen)

LPO = Lipooligosaccharide
(Has Lipid A and Core polysaccharide but NO O-ANTIGEN)

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17
Q

What are the conserved and variable regions of LPS?

A

Conserved = Structure of the core polysaccharide

Variable = Structure/composition of the O-antigen

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18
Q

What benefit do we get from the unique nature of the O-antigen on LPS being characteristic?

A

We can use it to IDENTIFY strains!

–> Used in SEROTYPING! Since each strain has a unique O-antigen on their LPS molecules, the Abs that bind to the O-antigens will differ!

–> We can identify strains based on this differential binding!

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19
Q

Serotyping

A

A diagnostic method using antibodies to identify + distinguish closely related strains by their surface antigens

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20
Q

Serotype

A

A strain of microbe identified via sertotyping

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21
Q

During infection, how/when does LPS get RELEASED from the OM?

A

1) During bacterial division

2) Upon bacterial lysis (death)

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22
Q

What happens when LPS is released?

A

They get recognized by TLRs on immune cells (of the innate immune system)

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23
Q

TLR

A

“Toll-Like Receptor”

–> Found on immune cells of the INNATE immune system (Ex: macrophages)

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24
Q

What part of LPS binds to the TLRs?

A

The Lipid A portion!

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25
What occurs upon binding of LPS to TLRs?
The Lipid A-TLR binding event triggers immune cells to release pro-inflammatory cytokines!
26
A low concentration of released LPS is ___________ to host
**low LPS conc** == **Beneficial** to host! --> Stimulates immune response in host that can PREVENT disease --> Triggers LOCALIZED inflammation allowing for the recruitment of immune cells to the specific area to fight the pathogens
27
A high concentration of released LPS is __________ for host
**high LPS conc* = **BAD** for host! --> When a lot of LPS is released SYSTEMICALLY, this can cause a systemic inflammatory resposne! == Can lead to septic shock and death!
28
Septic shock occuring due to LPS presence is commonly a result of?
Gram (-) infection getting into the bloodstream
29
How does N. Meningitis infection demonstrate the damage due to systemic LPS release?
If N. meningitis gets into bloodstream, it can travel to the CNS where it colonizes the meninges (spread due to systematic infection) --> Release of LPS in the meninges causes inflammation in these areas --> Inflammation = increased pressure = damages neurons! == leads to disease progression
30
How does N. gonorrhea infection demonstrate the damage due to systematic LPS release?
N. gonorrhea spreads into the fallopian tubes --> Releases LPS in the fallopian tubes causing damage to them == Results in sterility!
31
Other than LPS what are 2 other endotoxins?
1) LPO 2) LTA
32
In what bacteria is LPO usually found?
**Neisseria + Bordetella genera** (Gram (-) bacteria) (N. gonorrhea has it!)
33
LTA
Lipoteichoic Acid = A cell wall molecule anchored to the PM of **Gram (+)** cells --> Is functionall equivalent to LPS!
34
How is LTA functionally equivalent to LPS?
1) Binds to TLRs on immune cells 2) Triggers inflammatory response
35
What are the main biological effects (immune responses) triggered by LPS + LTA?
1) Fever 2) Inflammation 3) B-cell proliferation 4) Clotting cascade initiation
36
What is the intended protective effect of FEVER?
Inhibition of pathogen replication AND increased immune cell activity
37
What is the intended protective effect of INFLAMMATION?
Intended to allow for the transport of immune cells/molecules to infection sites! (to facilitate their movement!)
38
What is the intended protective effect of B-CELL PROLIFERATION?
Intended for antibody production (to begin generating the adaptive immune response)
39
What is the intended protective effect of CLOTTING CASCADE INITIATION?
Intended to prevent the spread of pathogens! --> Makes it harder for the pathogen to move through the thicker blood and blocking clots
40
AB Toxins
Two-component exotoxins possessing a receptor subunit (B) and an enzymatically active subunit (A)
41
AB Toxins are named after their...
structure! (composed of A + B subunits)
42
What are the main structural components of AB toxins? What does each part do?
**A subunit** = Enzymatically active peptide; usually responsible for carrying out the toxic effect **B subunit** = Membrane-binding portion (binds to host cell membrane via host receptors)
43
AB toxins are initially synthesized as...
Inactive precursors! (A+B subunits stuck together) --> Then get activated AFTER production!
44
What must occur to activate AB toxins?
They have to be cleaved in some way (separating A + B subunits)
45
Where/how does AB toxin activation occur?
Can take place either in the producing bacterial cell OR in the HOST cell! --> Occurs by protease cleaving the AB complex to release the subunits
46
What is the structure of the AB toxin for: Diptheria, Botilinum, Tetanus toxins?
1 A subunit + 1 B subunit
47
What is the structure of the AB toxin for: Shiga toxin and cholera toxin?
1 A subunit + multiple IDENTICAL B subunits
48
What is the structure of the AB toxin for: Pertussis?
1 A subunit + 5 DIFFERENT B subunits
49
What is the first challenge AB toxins must "overcome" in order to exert their toxic effects?
Gaining entry: Must get through the PM of the host cell! (too big to get through by itself)
50
How do AB toxins get through the host PM? main method?
Can use different methods BUT all typically rely on transport mechanisms of the HOST! Main Method = **Receptor-mediated endocytosis**
51
What determines the initiation of receptor-mediated endocytosis of AB toxin?
Binding of the B subunit to a host receptor! --> Triggers endocytosis!
52
The B subunit of the AB toxin determines what characteristics of the toxin? (2)
1) Tissue preference 2) Species specificity --> Because the B subunit will only bind receptors on specific cells!
53
Once an AB toxin is endoctosed, what must occur?
The A portion must escape the endosome in some way --> The main method for this is endosomal acidification
54
Diptheria ENTRY process:
1) Inactive diptheria precursor is made by bacterial cell and released into the ECF 2) B subunit of the diptheria toxin binds to diptheria receptors on the host cell surface == triggers endocytosis! 3) Receptor-bound diptheria is brought into the cell within an endosome 4) Acidification of the endosome causes conformational changes within the AB toxin == B subunit dissociates from A subunit AND the receptor 5) B subunit inserts into the endosomal membrane forming a CHANNEL! 6) The dissociated A subunit moves through this channel and enters the cytoplasm!
55
Diptheria TOXICITY process: (After entry what happens)
After escape from endosome: 1) Diptheria A peptide targets EF2 2) Diptheria A peptide acts upon EF2, ADP-ribosylating it! 3) ADP-ribosylated EF2 cannot function properly = improper mRNA binding 4) Without EF2-mRNA bindng, ribosomal initiation of translation cannot occur == Inhibition of protein synthesis! (eventually causing cell death)
56
What is the target of Diptheria?
EF2 --> Inactivates it to inhibit protein synthesis in host
57
What are the targets of Pertussis + Cholera toxins?
Both target G-signaling molecules! Pertussis = Gi Cholera = Gs
58
What do pertussis and cholera toxins do?
They **ADP-ribosylate G-signaling molecules** causing them to be "locked" in their activated state! == Maintains the function of adenylyl cyclase == Excessive cAMP production == **Causing Water/ion balance disruptions!**
59
What bacteria produce Shiga-like toxin?
Enteropathogenic E. coli (0157:H7)
60
What is the receptor for shiga toxin?
Gb3
61
What does shiga toxin do?
Its A subunit cleaves rRNA needed for proper ribosomal assembly == Ribosomes do not fully assemble, preventing translation == Inhibition of protein synthesis!
62
What toxins work by inhibiting protein synthesis?
1) Shiga-toxin 2) Diptheria-toxin
63
Where are Gb3 (shiga receptors) found within humans?
Mainly found in the KIDNEYS + Blood vessel lining!
64
What are the reservoir hosts of E. coli O157:H7? WHY
Sheep, cattle, pigs, deer == Can carry the 0157:H7 strains without being harmed because they LACK the shiga-toxin receptor!
65
What factors determine the degree of damage AB toxins induce?
1) Type of AB toxin present 2) # of AB toxins present (conc.) 3) Distribution of present AB toxins (localized, systematic, etc.)
66
What AB toxins directly CLEAVE host molecules?
1) Shiga toxin 2) Botulinum toxin 3) Tetanus toxin
67
Botulinum and tetanus toxins are BOTH... (list similarities too)
Potent neurotoxins! 1) Both act on SNARE proteins 2) Both alter the release of NTs from neurons
68
What are the SNARE proteins needed for normal NT exocytosis?
1) Synaptobrevin = IN the NT vesicle membrane 2) SNAP-25 = Connects synaptobrevin and syntaxin 3) Syntaxin = IN the neuronal PM
69
Cleavage of ANY SNARE protein causes...
Inhibition of NT release from neurons! (No vesicle-PM fusion event can occur)
70
What does SNARE stand for?
"Snap Receptor"
71
What is the primary role of SNARE proteins?
Mediate the fusion of vesicles with their target membrane-bound compartments
72
What is the molecular target of botulinum toxin?
A subunit of BT toxin cleaves SNARE proteins within motor neurons ( the specific snare cleaved depends on the type of BT toxin)
73
What is different in the targets of botulinum and tetanus toxins?
BT toxin = targets SNAREs in MOTOR neurons Tetanus toxin = targets SNARE in INHIBITORY neurons
74
What SNARE is cleaved by BT toxin Types A, C, E?
SNAP-25
75
What SNARE is cleaved by BT toxin Types B, D, F, G?
Synaptobrevin
76
What SNARE is cleaved by just BT toxin Type C?
Syntaxin
77
BT Toxin Process: (For type A)
1) BT toxin binds to receptor on motor neuron 2) BT toxin is endocytosed --> A subunit escapes endosome 3) BT toxin A peptide CLEAVES SNAP-25 4) Ach vesicle synaptobrevin cannot bind cleaved SNAP-25 == No linking of synaptobrevin to syntaxin 5) No membrane fusion occurs == No Ach release! (by exocytosis) 6) **No muscle contraction!**
78
79
What does the host organism experience due to BT toxin?
Flaccid Paralysis
80
Flaccid Paralysis
Extreme muscle weakness and loss of muscle tone
81
What is the molecular target of tetanus toxin?
Synaptobrevin (in GABA/glycine vesicles within inhibitory neurons)
82
What NTs do BT toxin and tetanus toxin impact the release of?
**BT Toxin** = Inhibits release of acetylcholine (Ach) **Tetanus Toxin** = Inhibits release of GABA or glycine (directly) == Indirectly promotes the release of Ach!
83
Tetanus Toxin Process:
1) Tetanus toxin B subunit binds to receptors on MOTOR neurons and get endocytosed 2) The A subunit of tetanus toxin escapes the endosome within the motor neuron 3) Tetanus-A subunit is transported from the motor neuron to the CNS where it is finally transported to **inhibitory neurons** 4) Within an inhibitory neuron, the A peptide cleaves synaptobrevin within the vesicles containing GABA/glycine 5) Without synaptobrevin, SNAP 25 and syntaxin cannot bind == no fusion of vesicle with the neuronal PM 6) No GABA or glycine is released == No inhibitory NTs bind to motor neuron 7) Motor neuron continues realeasing Ach without being able to stop == continual muscle contraction = SPASTIC PARALYSIS!
84
Spastic Paralysis
Unusual tightness/stiffness of muscles
85
Spastic and flaccid paralyses can be deadly if...
If respiratory muscles are impacted == SUFFOCATION!
86
What are two inhibitory NTs?
GABA + Glycine
87
Toxoids
Denatured AB toxins
88
What do we use toxoids for? Why?
Used in vaccines! We use them because they allow for the generation of protective Abs against the ACTIVE toxin but without containing the structure for toxicity (doesn't get us sick while we generate an immune response)
89
What are the 6 main AB toxins we studied? (+ their target)
1) Diptheria Toxin (EF2 = protein synth. inhibition) 2) Shiga Toxin (rRNA = protein sytnh. inhibition) 3) Pertussis Toxin (Gi = disrupt water/ion balance) 4) Cholera Toxin (Gs = disrupt water/ion balance) 5) Botulinum Toxin (SNAP-25 = inhibit muscle contraction) 6) Tetanus Toxin (synaptobrevin = continual muscle contraction)

BIO 315 (33 decks)

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