Salmonella enterica

Question 1

Range of salmonella?

Answer 1

Broad

Question 2

What dos it cause

Answer 2

Foodborne gastroenteretis, typhoid fever

Question 3

What is a serotype

Answer 3

Variation between species of vacteria for causing disease

Question 4

Typhoid serovars are

Answer 4

S. enterica, sub.enterica, typhi OR paratyphi
They are human-restricted

Question 5

Non-typhoid serovars are

Answer 5

S. enterica, sub. enterica, tiphimurium
Broad range
This is model to study in labs

Question 6

What are the problems of chronic carriage of salmonella (3)

Answer 6

1) bacteria shed toothers
2) antibiotics cannot clear everything
3) You can have salmonella ithout even knowing it

Question 7

Antibiotics towards S. enterica

Answer 7

Are mq (transcription)
macrolides
quinolones

Resistance is a problem

Question 8

Does drug resistance only occur in humans?

Answer 8

No, in envrionment as well

Question 9

What’s different between S. enteria, subs enterica, TYPHI and THYIMURIUM

Answer 9

Typhi (human restricted) has WAYYY more pseudogenes (non-functional proteins)

Question 10

What are the two pathogenicity islands that code for secretion systems

Answer 10

SPI1 and SPI2 code for T3SS, for early and late infection
Effector proteins are released through the T3SS

Question 11

What are the names of the vacuoles where Salmonella stays?

Answer 11

SCV

Question 12

Where does salmonella enter the body?

Answer 12

in the instestinal eptithilium.
Depending on the serotpye, it will enter different cells (usually non-phagocytic)

Question 13

What does SPI1 do?

Answer 13

promote entry into non-phagocytic cells

Question 14

What does SPI 2 do?

Answer 14

Promote surivival, replication and cell-cell spread

Question 15

Give the 5 steps of salmonella infection?

Answer 15

1. Before infection, it will trigger its early SPI-1 (T3SS) to deliver effector proteins to the host
   Allows the ruffle of the host membrane – allows bacteria to enter host, Vacuole is made
2. It will interact with the endocytic pathways
3. It will turn off SPI-1 and turn on SPI2.
4. It will then target the lysosomal pathway through its SPI2 effectors
5. There is also formation of tubules SITS. SITS are used to allow the bacteria to go back to the cell periphery

Question 16

How does salmonella enter non-phagocytic cells?

Answer 16

SPI1 T3SS will deliver effectors similar to host proteins

They will activate Rho GTPases. These will allow for cytoskeleton rearrangement

This will afterwards need to be turned off to complete uptake

Question 17

Which small GTPase allows for uptake to happen?

Answer 17

Rho (of Ras superfamily)

Question 18

4 effectors control uptake? What do they do?

Answer 18

3 of them activate GEF or they mimic GEF
One is a GAP mimic to turn off uptake

Question 19

How do SPI1 effectors suppress autophagy (sopF)

Answer 19

SopF of SPI1 tagets initiation of xenophagy. Xenophagy was discovered this way

vacuole ATPase is deactivated, o it can’t bind to a complex to start autophagy

Question 20

2 Reasons why SPI2 effectors control bacterial poisoning?

Answer 20

Intermediate infection: want to keep pathogen near Golgi for nutrient acquisition
Late infection: bring to cell periphery for cell-cell spread

Question 21

Which SPI(s) affect autopahgy

Answer 21

Both SPI1 and SPI2

Question 22

How do SseF and SseG contribute to intermediate infection?

Answer 22

They thetther the SCV to the Golgi membrane

Question 23

Which motor protein helps with movement towards cell periphery

Answer 23

kinesin

Question 24

What do GTPases on SCV do to help with movement

Answer 24

GTPases will bind to an adaptor protein to bind with either kinesin or dyenin

Question 25

How does SifA make cell movement stay towards the golgi?

Answer 25

Connects with dyenin adaptor BLOC2

Question 26

What is LAMP?

Answer 26

It’s a SCV marker

Question 27

What does PipB2 do to make cell movement towards periphery? (2)

Answer 27

Interacts directly with kinesin adaptor SKIP
Interacts with light chain of kinesin itself

Question 28

What is a SIT? What are their possible purposes?

Answer 28

salmonella induced microtubule
Cell spread, nutrient acquisition

Question 29

Which effectors cause SIT (5)

Answer 29

SifA, PipB2, SOPD2 = manipulate host microtubules

SseF and SSeG = tethering to Golgi

Question 30

How do SPI2 effectors SseF and SseG target autophagy?

Answer 30

They bind to Rab1 GTPase to inihibit an initiation complex

Question 31

How does salmonella effectors target NFkB pathway? (2 proteins)

Answer 31

It inhibits gene expression by cleaving proteins of pathway p65 and RelB

Question 32

How does SPI2 effectors suppress antigen presentation in DENDRITIC cells?

Answer 32

Affect microtubule formation - prevents loading from happening

Salmonella effectors affect MANY types of cells.

Question 33

Evolution of SPI1 and SPI2 in enterica vs. bongori

Answer 33

SP1 is in both
SP2 is unique to enterica

Question 34

What happened to effector proteins in typhi serotype?

Answer 34

Lost function of effectors - make it unique to human infections

Question 35

Which GTPase is related to host broadness. What do the 2 effectors do to it?

Answer 35

Rab32
Effectors sopD2 and gtgE target Rab32 to stop it from working

Question 36

What is special about typhi’s SopD2 and gtgE?

Answer 36

They are knocked OUT
So, for BROADNESS of hosts in typhiMURIUM, these two are requried

Question 37

How does SopD2 of typhiMURIUM affect Rab32, to allow for host BROADNESS?

Answer 37

SopD2 acts as a GAP to inactivate Rab32 GTPase

Question 38

How does s. TYPHI use virulence factors to target HUMANs only? (2 ways)

Answer 38

Has polysaccharide capsules (Vi antigen) on surface to evade immune detection

Secretes a Typhoid toxin (CdtB exotoxin) that causes DNA damage tp human cell targets specifially