L13 - Shigella and Listeria Flashcards
name the type of bacteria that shigella and listeria are
facultivea intracellular
= can live and replicate inside and outside of host cell
simple pathogensis of shigella and listeria
ingested in contaminated food
pass through M-cells in Small intestine
engulfed by macrophages on other side but escape vesicle and proliferate in cytoplasm
= can also tirck normal cells to take them in = alternatrive route to M-cells
who discovered shigella
Kiyoshi Shiga
caused diarrhoea when he fed isolated bacteria to dogs
gram stain of shigella
negative
symptoms of shigellosis
Bloody diarrhea
fever and stomach cramps
worldwide deaths from shigella/shigelliosis annually
600,000
most commonly infected by shigella and how
infants and childeren in 3rd world countries
infected water - feral-oral
what is the ID50 of shigella
5 bacteria
= very low
ID50 = number of bacteria required to cause disease/infection
history of Listeria
origanlly named ‘bacterium’
later chnaged to ‘listeria’ in 1940
describe shape and gram of listeria
gram positive rods
contains flagella at lower temperatures
how is listeriosis/listeria transmitted and who to mainly
conbtaminated food
= milk products - cheese
people with wekaned immune system (pregnant,neborns)
temperature prefferences of listeria
can still grow at low temps
and displays high heat reistance
= most virulence factors upregulated at 37˚
what is the ID50 of listeria
10^3
much higher than shigella
what part of the body does listeria infect
has access to bloodstream and lymph circulation after crossing intestinal barrier= wide range of targets
= can cross placental barrier and infect foetus
= can cross blood-brain barrier
what are the 4 stages that all intracellular bacteria undergo
- entry/invasion
- exapse from vacuole
- replication in cytoplasm
- mannipulation of innate responses triggered in cytoplasm
describe Listerias ‘Zipper’ mechanism to invade host cells
tricks non-phagocytotic cells to ‘engulf’ listeria
- adhesins bidn to receptors
- membrane engulment vai membrane protrusion
= pseuodpodia
describe the ‘Trigger’ mechansim used by Shigella to invade host cells
T3SS used in same way as salmonella
- T3SS injects effector proteins
- cause membrane shiffling by affecting Rac1 GTPase
= produces filopodia/protrusions that disrupt membrane
3.Shigella enters
at what temperature are shigella and listerias virulence factors unregulated
37˚
= but different mechanisms for detction and upregulatation
describe the mechanims shigella undergoes to upregulate virulence factors when temp is above 37˚
- high temp activates DNA gyrase to modulate supercoiling/open DNA
- VirF is produced
- VirF activates VirB = T3SS operon
= codes for structurala nd effector proteins
describe listerias mechanisms to upregulate virulence factors above 37˚
RNA thermosenser
= prfA is a transcription factor for virlulence genes
- at low temps PrfA mRNA forms a secondary strcuture blocking ribosome binding site
- at high temps prfA undergoes comformational change
= can bind and be translated
- virulence factors are transcibed
why must listeria and shigella repaidly escape endosome/vaccuole
before lysosome fuses and kills bacteria within endosome
name the 2 enzymes involved in the excape from vaccuole/endosome in listeria
Listeriolysin O (LLO)
Type C phospholipase (PLC)
describe emchansim of escape from endosme by listeria (LLO + PLC)
- acidic conditions of vacuole activate Listeriolysin-O (LLO)
- binds ot cholesterol and forms pore
= membrane disruption
- PLC helps disruption of vacuole + is important in double-membrane disruption
= cell-cell spread
role of actA in listerias lifecycle inside cytoplasm
after listeria has escaped from vacuole and free inc cytoplasm
- actA binds and wraps around bacteria
- recruits proteins produced by host cell
= disguises bacteria by hiding within host proteins
- produces actin commet tail to move around cell or to new host cell
what happens if there are mutations in actA - listeria
no coating of host proteins to listeria = no ‘disguise’
recognised and ubiquitinated
= destroyed by host cell
mechansism of vacuole escape - shigella
- IpaB and IpaC are injceted into cytoplasm
= form pore complex
- disrupt phagosomal membrane = escape
what is IscA from shigella similarv to in function in listeria
actA
= both form polymerisation of `actin to form ‘actin-commet’
role of IscB in shigella (think of IscA)
iscB is recruited to IscA and hides it
= cannot be targetted by autophagy pathway
= no IscB = autolysosome forms and destroys bacteria
summarise shiggella vs listerias diuffernt poroteins and pathways for:
1.entry
2.lysis of vaccuole/escape
3. cell-cell spread
- Entry:
listeria - adhesins - ‘zipper’ mechansim’
shigella - T3SS - Lysis:
listeria - LLO + low pH
shigella - T3SS - IpaB + IpaC
movement:
listeria - ActA
shigella - IscA
