microbes and the immune system Flashcards
what are the microorganisms
1-photoautotroph
2-chemoheterotroph
3-photoheteretroph
4-chemoautotroph
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
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
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
how does cryoprotectants help bacteria survive at different temperatures?
cold/ heat shock proteins. prevents proteins unfolding/ denaturing to maintain correct structure and activity.
describe the two ways to sequence bacteria for
-16S sequencing
-whole genome sequencing
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
how do we obtain short chain fatty acids in colon and what is there function with an example?
produced by bacterial fermentation of dietary fibre from plants.
they are the main energy source for epithelial cells
how was clostridium difficile infection treated?
faecal tranplant
what is the bodies initial response to infection - acute inflammation
activation of local irate immune cells
increase permeability of local blood vessels
immune cells and plasma protein migrate into tissues
how are PAMP (pathogen associated molecular patterns) on all pathogens recognised by immune system?
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
what type of pathogen can hide from PRR by reducing recognition of TLRs using TLR5
heliocobacter pylori
how does PRR activation of TLR warn the immune response about the infection?
TLR activation activates NF-kB. this alters gene transcription, but allows cell to warn the immune system
what damage signals does PAMP receive to identify hosts ?
DAMPs - released by dying cells due to damage of tissue from pathogen
describe two causes of antibiotic resistance
1) overprescribing of antibiotics
2) over use and misuse of antibiotics in livestock and fish farming
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
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
- 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.
explain the B-Lactam antibiotic
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
how does antibiotic resistance develop in bacteria.
-two types of resistance?
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