Bacterial infection 2 Flashcards
Invasion
Pathogen moving into or through mucosal epithelium
to reach site of infection
Biofilm
- define
= surface-associated multicellular communities
in host tissues or medical devices
Cells embedded in exopolymeric matrix
Biofilm formation
- role
Protection from enviro stress
e.g IS or ABs
EPEC main site of infection
Mucosal membrane
Invasion
- 3 options for a bacterial cell that’s attached themselves to an epithelial cell
>Enter host cells + pass through >Move between host cells - disrupt tight junctions = more permeable >Intracellular = remain within cells
Intracellular invasion
Enter host cells
Survive within host cells
Move through host cells
- > exit cells
- > spread to other cells
(Need to be able to overcome our systems to exclude them)
Mechanisms for entry into host cells
Active mechanisms
= zipper + trigger
Induce uptake by host
Zipper + trigger cause
Cytoskeleton reorganisation (actin) -> changes cell shape
Zipper
Exploits host cell receptors used for normal functions
- e.g. E-cadherin important in forming junctions between cells
Signals to host cell proteins
- > induces polymerisation of actin
- > forms endosome
- > engulfs bacteria
Trigger
T3SS- dependent
Inject efforts into host cells
- > trigger host cytoskeleton reorganisation
- > forms phagocytic cup
- > internalises bacteria
Trigger
e.g. Salmonella
Encoded on PAI 1 (=SPI-1)
Encodes 13 effectors
Phagocytosis
Inhibit bacteria growth:
- nutrient limited + acidic
Fuse w/ lysosomes
-> releases lysozyme, proteases + defensives into phagosome
= destruction
3 strategies to surviving inside host cell
- Adapted to survive phagosome-lysosome fusion
- Break out of phagosome before lysosome fusion
- Prevent lysosome fusion
Salmonella intracellular survival by…
Blocks maturation of phagosome
+ fusion w/ lysosome
Forms a SCV
= Salmonella Containing Vacuole
SPI 2 encodes…
= Salmonella PAI 2
Encodes functions that allow pathogen to alter phagosome properties
A T3SS + effectors infected into cell
- can prevent lysosome fusion
SPI-2 effectors
- when injected into host cytoplasm…
- Can initiate apoptosis
- Can down regulate inflammation
- Can modify surface of SCV
-> lysosome fusion blocked
(+ bacteria can exit cell when vesicle fuses w/ cell periphery)
SPI 1 + 2
Have to be coordinated to the different stages of infection
-> so use the right virulence factors at the right time
Escape from phagosome into cytoplasm
- L. monocytogenes
Encodes Listeriolysin O (LLO)
At pH 5.5. in phagosome
–> LLO forms pore in phagosome membrane
Works with phospholipase enzymes to break open phagosome
How Listeria spread to adjacent cells
Listeria then polymerise host cel actin
-> propel through cytoplasm
Q fever
- caused by
- transmission
Coxiella burnetii
Transmitted by deer ticks, illation, ingestion, wound contamination
Coxiella burnetii
- features
Obligate intracellular pathogen
Allows lysosome fusion
-> adapted to grow in acidic + nutrient-limited conditions
Modifies phagosome
= Coxiella Containing Vacuole
(CCV)
Coxiella burnetii
- effects on CCV
Expands CCV by fusion w/ other CCVs + endoscope
= Large Cell Variant (LCV)
Can be dramatic + take up lots of cell volume
Coxiella burnetii
- promotes cell survival
Suppresses apoptosis
Life cycle of Chlamydiae
Elementary body
= infectious form
- metabolically inactive
Reticulate body
= replicative form
- metabolically active
