Enteric Pathogens Flashcards
What do SPI-1 encoded T3SSs secrete?
Effectors SipB and SipC which modify the host cytoskeleton and effect actin polymerization so the Salmonella is engulfed my pseudopodia + internalised across the gut wall. Salmonella then exists within a SCV (Salmonella Containing Vacuole) kept alive by SPI-1 and SPI-2 encoded effectors.
What do the T3SS encoded by SPI-2 do?
Secrete effectors for intracellular growth within SCVs and resistance to NADH oxidase activity
How does Salmonella typhi survive within macrophages?
In a non-replicating state, preventing the phagolysosome from killing them by secreting 25 different effectors from T3SS
How many T3SS does Salmonella enteritidis use and what for?
Salmonella enteritidis remains restricted to the gut wall. It uses two T3SS, one to invade, one to spread.
What do effectors from SPI-3 and SPI-4 do?
Aid survival within macrophages
What do SPI-5 encoded effectors do?
They cause gut inflammation (enteritis) and fluid loss - symptoms of infection
What SPI-2 effector regulates T3SS expression in response to changes in pH
SSrB - a RNS sensitive effector that controls T3SS expression in response to low pH within macrophage phagolysosomes
How many T3SS does Salmonella typhi use and what for?
Salmonella typhi uses 3 T3SS to invade and spread systematically via the lymphatic system to cause Typhoid
Which regions of the E.coli K12 genome are not present in the EHEC genome and confer Shiga toxin virulence
Deletion of the non-pathogenic region between CadA and MelA which contributes to EHEC virulence
What did Lawrence et al. (1998) do?
Looked at the amount of horizontally transferred DNA in the E. coli genome and estimated the age of each region’s acquisition by looking at codon usage (different bacteria have different preferred codon usages)
Over time, acquired genes are likely to become more like the preferred codon usage of a bacterium if they are selected for as then they can be more easily translated
To become EIEC which genes must non-pathogenic strains acquire and which genes must it lose?
To become EIEC, a strain must acquire essential virulence genes called pINV and virulence enhancers called SHI.
It must lose the virulence suppressor CadA and lac genes (pathogenic E.coli is non-lactose fermenting/pale on MacConkey agar)
What colour does non-pathogenic E.coli grow on MacConkey agar and why?
Non-pathogenic K12 E.coli grows red colonies on MacConkey agar as it is lactose fermenting (lac genes are present)
What is the size difference between the genome of K12 and 0157H7 EHEC?
K12 is 4.6Mb, 0157H7 EHEC is nearly 5.6Mb
K12 is nearly 1 Mb smaller as EHEC has acquired many genes that allow it to: colonise the gut, adhere to the gut wall and damage host cells by secreting Shiga toxin
Which enteric pathogens secrete Shiga toxin (stx) and what is its structure?
EHEC and Shingella produce stx, it consists of 1 a subunit (toxin encoded by stxA) and 5 B subunits (encoded by stxB) in a pentameric ring
How does Shiga toxin enter cells and cause damage?
The B toxin subunits bind to Gb3 receptors and deliver the A subunit, once inside the cell the toxin is nicked and activated. It then binds to the 60S ribosomal subunit to prevent translation.
