LECTURE - Listeria Flashcards
Listeria monocytogenes is motile at these temperatures
20 degrees C by polar flagella
37 degrees C by causing actin polymerization within target cells
T or F. L. monocytogenes can form biofilms
T!
One of the few organisms that can cross the placenta
Listeria monocytogenes
This mediates L. monocytogenes attachment and internalization
Internalin A and Internalin B
- InlA binds to mammalian receptor E-cadherin and is sufficient for invasion of cells in the intestines
- it is also required along with InlB for invasion of the placenta (likely in brain microvessels as well to cause meningitis)
Inl B needs to bind to this receptor for hepatocyte growth factor (HGF) and is required for invasion of cells in placenta
Met
Listeriolysin O
- b hemolysis on BAP
- pore-forming toxin; to escape phagosome and grow in cytoplasm of infected cells
- LLO mutants have LD50 that’s 10^5 higher than wild type; mutants can’t survive in macrophages
These are important in limiting spread of L. monocytogenes
CD8+ cytotoxic T lymphocytes and NK cells (intracellular organism); intracell growth of listeria outside an endosome or phagosome triggers this response
____ expression is important as it activates macrophages and this will kill Listeria
IFN-y
wide range of temperature growth for L. monocytogenes
4 to 40 degrees C
room temp to refrigerated temps (enhances infective dose)
why does L. monocytogenes growth look like an umbrella?
organisms swimming up looking for better O2 levels
Large number of ingested organisms of Listeria is required to cause disease in adults
10^9
incubation period of listeria
30 days on average
- if stomach pH is raised, infectious dose can be lowered
Why does pregnancy increase susceptibility to listeria infection?
likely due to a switch in Th2-response predominantly
- intracellular pathogen SHOULD elicit Th1 response
Why does pregnancy increase susceptibility to listeria infection?
likely due to a switch in Th2-response predominantly
- intracellular pathogen SHOULD elicit Th1 response
fatality rate of Listeriosis
20-30%
ActA
- actin nucleator
- on surface of listeria
- focus for nucleation of actin filaments which propel bacteria through cytoplasm of host cell
- has to be phosphorylated to be active; may be localized to one pole of the bacterial cell
phosphoinositol-specific phospholipase C (plcA)
& phosphatidylcholine (non-specific) phospholipase C (plcB)
- Listeria hemolysins (as is LLO)
- act synergistically; 500 fold reduction in virulence if both are missing
PlcA
involved in the escape from primary phagocytic vacuole
PlcB
involved in the escape from the double membrane vacuole
- requires cleavage by Mpl, a zinc-dependent protease, for activity in supernatants
PlcA and PlcB
both can affect signal transduction in cells by releasing either diacylglycerol or ceramide from their target molecules, affecting Ca2+ release, and altering expression of the signal transduction molecules MAP-kinase and NF-kB
T or F. Listeria invasion across placenta involves internalin B and leads to septicemia
T!
This is probably not necessary for ingestion of bacteria by macrophage-like cells which are naturally phagocytic, but is essential for invasion of cells like enterocytes
InlA
two-step invasion and intracellular spread of Listeria happens in these cells
macrophages, liver cells, endothelial cells, enterocytes
this encodes for LLO
hly
