Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medical Microbiology > Bacterial Pathogens and Disease II-Endotoxins > Flashcards

Bacterial Pathogens and Disease II-Endotoxins Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards USMLE® Step 1 flashcards
1
Q
  1. What are endotoxins a component of?
A

•Endotoxins are a component (lipopolysaccharide) of the bacterial polysaccharide wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. What is the difference between gram + and gram - plasma membranes?
A

Both gram – and gram + bacteria have a plasma membrane. Gram + only have a outer peptidylglycan layer whilst gram – also have a second membrane (which contains lipopolysaccharides - endotoxins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. What three sections of lipopolysaccharides are there?
A
  1. Lipid A component
  2. Core polysaccharide component
  3. O side chain component
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. What is the lipid A component structure?
  • hydrophobic or hydrophilic?
  • Constant or species dependant?
A

2 phosphorylated glucosamines attached to long chains of fatty acids that sticks into the outer membrane for anchorage.
o Hydrophobic and the number/type of fatty acids are species dependent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  1. What is the core polysaccharide component structure?
  • hydrophobic or hydrophilic?
  • Constant or species dependant?
A 
unusual sugars (Ketodeoxyoctanoic acid (KDO) and heptose).
o	Hydrophilic and relatively constant between species of bacteria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. What is the O side chain component structure ?
    - hydrophobic or hydrophilic?
    - Constant or species dependant?
A

: Repeat units of tri, tetra or pentasaccharide sugars

o Hydrophilic, highly variable between species and very antigenically potent chain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. What component of the lipopolysaccharide drives septic shock?
A

The lipid A component

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Do immunogenic components drive septic shock?
A

no

The lipid A component does

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. Which component of the lipopolysaccharide is highly immunogenic and immune specific?
    - > What does this mean?
A

The O antigen is highly immunogenic ( easily provoke an immune response) and immune specific (only 1 antibody will be able to recognise this antibody)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. List three characteristics of lipopolysaccharides?
A
  1. Only present in gram negative bacteria
  2. Heat stable
  3. Not converted to toxoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. Which pathway do endotoxins initiate?
A

Sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. What is sepsis?
A

Life threatening organ dysfunction caused by a dysregulated host immune response to infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. Explain how sepsis is driven by the innate immune system- briefly?
A
  1. PAMP’s (eg endotoxins) + DAMP’s (from damaged host cells) detected via receptors
  2. Innate immune response driven
  3. Gene expression changed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. What does PAMP’s and DAMP’s stand for?
A

PAMPs = Pathogen associated molecular patterns

DAMPs = Damage associated molecular patterns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. What two types of receptors detect PAMPs and DAMPs and give examples of each?
A
  1. Cell membrane receptors - eg Toll like receptors (TLR) or C-type Lectin receptors
  2. Cytosol receptors - NOD like receptors and RIG-I like receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. Like some examples of cells that are apart of the innate immune system?
A
  • Macrophages
  • Monocytes
  • Granulocytes
  • Natural Killer Cells
  • Dendritic Cells
17
Q
  1. What are the 2 main effects of changing gene expression - (sepsis )??
A
  1. Production of pro-inflammatory cytokines (TNF-alpha, IL-1 and IL-6)—-> Recruits an immune response
  2. Inflammasomes to produce IL-1beta and IL-18 —> Rapid programmed cell death
18
Q
  1. What is the mechanism by which endotoxins (specifically Lipid A component) result in an increased pro-inflammatory cytokines and TNF-alpha?
A
  • Lipid A component is recognised by MD-2 so it binds to the lipopolysaccharide.
  • This complex then binds to the toll-like receptor which has a coreceptor called CD14.
  • This causes dimerisation of the receptor which results in intracellular signalling cascade.
  • This activates NF-kB which results in the production of TNF-a and other pro-inflammatory cytokines.
19
Q
  1. What are 7 effects of pro-inflammatory cytokines?

Out of these 7 effects, which three form a thrombus (immunothrombus)

A
  1. Increase number, lifespan and activation state of innate immune cells.
  2. Increase adhesion molecule and chemokine expression by endothelial cells.
  3. Increase acute phase proteins such as complement, fibrinogen and CRP (C-reactive proteins).
  4. Pro-inflammatory cytokines cause fever.
  5. Causes neutrophils to release extra-cellular traps (NETs) made of DNA and antimicrobial proteins that forms a scaffold for platelet activation.
  6. Cause release of microparticles by activated platelets
  7. Increase tissue factor expression by blood monocytes

5,6,7 = thrombus

20
Q
  1. What is a thrombus, what is the result of a thrombus?
A

A thrombus is a blood clot that forms in a vessel and remains there, microbes are trapped within the thrombus —–> attracts and activates further leucocytes

21
Q
  1. What are the 4 ways that lipopolysaccharides act as immunostimulants?

(rapid control of localised and minor infections achieved)

A
  • LPS stimulates macrophages to produce TNF which causes fever and reduces iron (to limit bacterial growth).
  • LPS activates receptors on endothelial cells to increase permeability (hypotension leads to septic shock).
  • LPS causes mast cells to degranulate and release inflammatory mediators.
  • LPS activates platelets, clotting and complement.
22
Q
  1. How might LPS cause organ failure
A

• Organ failure due to increased permeability, hypotension and hypovolaemic shock, fever, disseminated intravascular coagulation and multiple organ failure.

23
Q
  1. What happens if the process of LPS acting as immunostimulants passes a certain threshold?
A

Systemic Injury

24
Q
  1. How might immune dysregulation result in sepsis?

4 ways

A
  1. Production of ROS eg hydroxyl or NO
  2. Complement Action (especially C5a)
  3. Widespread immunothrombin
  4. Impaired mitochondria
25
Q
  1. How might the production of ROS (eg Hydroxyl or NO) result in sepsis?
A
  • > Damages cellular proteins
  • > Damages DNA and Lipids
  • > Impairs Mitochondria
26
Q
  1. How might the complement action( esp C5a) result in sepsis?
A

increase ROS

granulocyte enzyme release

endothelial permeability

tissue factor expression.

27
Q
  1. How might widespread immunothrombosis result in sepsis?
A

Widespread immunothrombosis leading to disseminated intravascular coagulation (DIC) with impaired microvasculature function and organ dysfunction

28
Q
  1. How might mitochondrial damage result in sepsis?
A

Mitochondrial damage leads to decreased intracellular ATP and cells enter state of hibernation – exacerbates organ dysfunction.

29
Q
  1. What are some resolutions of sepsis?
A

•Active negatively regulated process – not passive.

•Anti-inflammatory IL-10 produced early in process:
o Supresses production IL-6 and γ-interferon
o Stimulates production of soluble TNF receptor and IL-1 receptor antagonist

  • Autophagy of PAMP’s and DAMP’s – removal
  • Damaged cells undergo apoptosis and engulfment by macrophages.
30
Q
  1. A type of sepsis is called Meningococcal sepsis, what is this sepsis caused by?
A

•Caused by Neisseria meningitidis, a gram negative diplococcus

31
Q
  1. What are the different serotypes (strains) of Neisseria meningitidis
A

•Serotypes A,B,C, Y, W135

32
Q
  1. Where is the serotype A of Neisseria meningitidis predominantly found?
A

• Serotype A associated with large outbreaks in Sahel region of Africa – Meningitis belt.

33
Q
  1. Which serotypes of Neisseria Meningitidis are found in the uk?
A

Serotype B, C and W135

34
Q
  1. Which vaccines have caused a decrease in the serotypes B,C and W135 in the Uk?
A

MenC and now MenB vaccine.

35
Q
  1. What is the range of diseases that Neisseria meningitidis can cause?
A

•Can cause disease ranging from meningitis to life threatening meningococcal sepsis.

36
Q

36.What makes meningococcus so effective in sepsis?

A
  1. Hexa-acylated Lipid A (more toxic than penta-acylated) and terminal residue mimicry of host antigen (has a very short O antigen component)
  2. Blebs parts of the membrane that are full of LPS and lipid A component – overwhelming immune response due to this

Medical Microbiology (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions