microbes and the immune system Flashcards

1
Q

what are the microorganisms
1-photoautotroph
2-chemoheterotroph
3-photoheteretroph
4-chemoautotroph

A

1- uses energy as sunlight to convert co2 to carbs
2- uses organic chemical substances as energy source and organic substances as carbon
3- use light for energy but cannot use co2 as carbon source
4-chemoautotroph- uses inorganic chemicals as energy source to convert to organic compounds

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2
Q

name 5 temperature organisms to allow bacteria to survive in different environments ?
1) psychrophiles (unsaturated fat)
2) mesophile
3) thermophile
4) hyperthemophile (saturated fat)
5) extremophile

A

1) survive <15 degrees. good fat= liquid. increase in unsaturated fats to allow fluid
2) human pathogens at body temp of 37 degrees
3) used as biological indicator
4) hyperthermophile- survive >70 degrees. good fat = solid. increase saturated fat to maintain shape.
5) extremophile- survive in extreme cold temperatures

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3
Q

how does cryoprotectants help bacteria survive at different temperatures?

A

cold/ heat shock proteins. prevents proteins unfolding/ denaturing to maintain correct structure and activity.

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4
Q

describe the two ways to sequence bacteria for
-16S sequencing
-whole genome sequencing

A

16S- bacterial DNA that encoded rRNA molecule. can identify species and relative frequencies

WGS- total microbiome DNA sequencing can fnd mutations, SNPs and better understanding of population

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5
Q

how do we obtain short chain fatty acids in colon and what is there function with an example?

A

produced by bacterial fermentation of dietary fibre from plants.
they are the main energy source for epithelial cells

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6
Q

how was clostridium difficile infection treated?

A

faecal tranplant

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7
Q

what is the bodies initial response to infection - acute inflammation

A

activation of local irate immune cells
increase permeability of local blood vessels
immune cells and plasma protein migrate into tissues

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8
Q

how are PAMP (pathogen associated molecular patterns) on all pathogens recognised by immune system?

A

recognised by pattern recognition receptors (PRR) on cells on the immune system and epithelial cells
different PRR are found on different cells e.g. TLR recognise PAMP on cell membrane.
occurs in cytoplasm

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9
Q

what type of pathogen can hide from PRR by reducing recognition of TLRs using TLR5

A

heliocobacter pylori

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10
Q

how does PRR activation of TLR warn the immune response about the infection?

A

TLR activation activates NF-kB. this alters gene transcription, but allows cell to warn the immune system

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11
Q

what damage signals does PAMP receive to identify hosts ?

A

DAMPs - released by dying cells due to damage of tissue from pathogen

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12
Q

describe two causes of antibiotic resistance
1) overprescribing of antibiotics
2) over use and misuse of antibiotics in livestock and fish farming

A

1) 20% of antibiotics prescriptions in primary care are estimated to be unnecessary
2) 70% of antibiotics are consumed by animals.
how animals can pass on resistant bacteria=
direct contact from animals to farmers
consumption of meat from animals
through the environment

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13
Q

describe how antibiotics work in each stage
-nucleic acid synthesis
-target ribosomal function
-target cell wall
-target cell membrane
-inihibition of cell metabolism and growth

A
  • targets machinery that makes DNA and RNA
    -targets the machinery that produces proteins
    -target the synthesis of cell wall e.g. chop up or stop being made
    -outer membrane of gram negative and inner of gram positive.
    -inhibit folic acid biosynthesis and oxidative phosphorylation of ATP synthase.
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14
Q

explain the B-Lactam antibiotic

A

binds to prenecillian binding proteins (PBP).
the function is to build structure of cell wall in bacteria, which prevents the cross-linking of peptidoglycan layer of bacterial cell wall.
the bacteria swells, reputures and dies due to osmotic gradient.

however bacteria can change their binding protein to prevent B-lactam working

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15
Q

how does antibiotic resistance develop in bacteria.
-two types of resistance?

A

1) intrinsic : evolution by changing their structure or components. occured before antbiotic treatment began.
2) acquired: bacteria develop resistance to antibiotics. induced after therapy e.g. random mutation or acquired DNA that encodes for antibiotic resistance

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16
Q

what are two mechanisms for intrinsic and acquired resistance?

A

1) reduced drug uptake

2) enzymatic degradation

3) target modification= bacteria changes antibiotic that reduces the binding affinity with therapeutic targets.

4) increased drug efflux

17
Q

how quickly does antibiotic resistance develop

A

depends on how much antibiotic being used. using too much or too little increases antibiotic restitence.
using correct amount the bacteria cannot win;
100x MIC after 11 days

18
Q

example of complement cascade system in innate immune system to control pathogens
-C3a and C5a
-C3b
C5-C9

A

C3a and C5a = released at site of infection to activate acute inflammatory response by increased immune cells

C3b= improved phagocytosis leads to faster clearance and killing of pathogen e.g. small pox inactivates this

C5-C9= forms membrane attack complex MAC. which kills pathogens

19
Q

examples of how host cells and pathogens evade complements
-CD46
-CD59
-C1 inhibitor
-express CRIT

A
  • CD46= inactivates C3b e.g. small pox
    -CD59= stops MAC from forming

c1 inhibitor = stop immune response e.g. e.coli

express CRIT= blocks early steps in complement activation e.g. trypanosoma

20
Q

Which of the following microbes can be found in both the Stomach and the Small Bowel System

A

lactobacilli

21
Q

how are Lymphocyte antigen specific receptors best characterised

A

millions of different receptors are generated through gene rearrangement

22
Q

What makes plasmids particularly effective in enhancing bacterial virulence?

A

Their mobility and capacity to carry genes for toxins and antibiotic resistance.

23
Q

role of quorum sensing in biofilm formation

A

quorum sensing= cell to cell communication of bacteria to share information.
triggers production of signalling molecules that coordinate extracellular matrix production

24
Q

consequence of prolonged antibiotic use on the gut microbiota

A

colonisation of opportunistic pathogen

25
Q
A