Lecture 21 - Bacterial invasion Flashcards
(18 cards)
list the 3 definitions of invasiveness
- enter, grow and reproduce in host then spread
- Entry and survival within phagocytes
- enter non-phagocytic host cells
how do bacteria enter/grow/reproduce/spread? give 4 examples
- spreading factors that alter/dmg tissue
1. collagenase by clostridium
2. fibrinolysin by staph
3. hyaluronidase by strep
4. DNase by all = destroys DNA and lowers viscosity of exudate for motility
how do phagocytes kill bacteria and what 3 ways can bacteria evade it?
- phagosome fuses with enzymatic lysosome
1. resistant to phagolysosome
2. prevent fusion
3. escape into cytoplasm
what happens when bacteria invade non-phagocytes? how do bacteria force uptake?
- invasion = colonise mucosa, translocate to deeper tissue, systemic
- force = invasins rearrange cytoskeleton = pseudopod
what are the benefits of invasion?
safe = nutrients, no competition, evade immunity and antibiotics
explain zipper invasion and list 2 examples
- invasins bind = actin polymerisation -> pseudopod
- eg Listeria and yersinia
explain trigger invasion and list 2 examples
- T3SS effector injection = activates actin -> membrane ruffling and uptake
- eg shigella and salmonella
briefly describe listeria
G+ve rod, facultative intracellular in phagocytes, food borne, liver and epithelia
describe the 7 step process of listeria zipper invasion
- internalin InIB binds host Mesenchymal epithelial transition factor (Met) = cell survival
- signal transduction to actin related protein (ARP) 2/3 complex
- ARP 2/3 = G and F actin assembly for uptake
- listeriolysin O haemolysin lyses vacuoles = escape to cytoplasm
- ActA activates ARP 2/3 for de/polymerising actin into tails for motility
- push into adj cell then bud off into vacuole
- lyse vacuole etc for cell-cell spread
briefly describe shigella
G-ve rods, haemorrhagic dysentry + abscesses + ulcers
Describe the 8 step trigger invasion of shigella
- microfold (M) cells take up and translocate
- endocytosed by resident macrophages
- escape phagosome and induce macrophage death = release
- induce actin polymerisation = engulfed into enterocytes basolaterally
- lyse vacuole = escape into cytoplasm
- actin motility like listeria
- push into adj cell then bud off
- lyse vacuole for cell-cell spread
briefly describe salmonella
G-ve rods, T3SS to small intestine, typhoid and enterocolitis, contaminated water/animal products
describe the 4 step trigger invasion of salmonella
- T3SS = membrane ruffling and uptake
- vacuole translocation by host microtubules
- released into underlying tissue
- phagocytosed, prevent fusion, disseminate
compare salmonella from shigella (4 points)
- invade from lumen not M cells
- survive in phagocytes not lyse them
- disseminate not cell-cell spread
- strong inflammation
which 2 bacteria use T3SS for trigger invasion?
shigella and salmonella
list the 5 functions of the effector proteins by T3SS in shigella
- IpaB adhesin binds CD44 on basolateral colon epithelia
- IpaB as T3SS tip complex
- IpaC interacts with B to insert in host PM as pore
- IpaC, IpgB1 B2 and D = actin polymerisation
- IpaA = actin depolymerisation
describe the similarities of listeria and shigella in 1 specific aspect
- haemolysins for after escaping phagosome
- listeriolysin O = binds cholesterol version
- IpaB/IpaC = pore forming version
compare listeria, shigella and salmonella
- listeria = zipper by invasins, actin motility
- shigella = trigger by T3SS, actin motility
- salmonella = trigger by T3SS, intracellular in phagocytes
