African tryps and tsetse fly interactions Flashcards
What do tsetse feed on?
Blood ONLY- obligate blood feeders.
What is the animal trypanosomiasis called? What are its repercussions?
Nagana.
Contributes to poverty by preventing farming and causing economic losses.
How are tryps obligate in blood?
Allowed by VSG switching
How does VSG work? Why is it only effective at low immune titres?
Clears Abs on parasite surface (when immune titre isnt high). When titre is high, complement system is activated which destroys parasites.
as well as allows evasion of immune system.
How is tryp pleiomorphic?
Short stumpy form which cannot express VSG when ready for trasnmision into insect.
Long slender form when in exponential growth phase in humans.
Considering markers, how does slender switch into stumpy?
Some markers expressed in stumpy but REPRESSED in slender form.
Protein expressed in in stumpy is a family of transporter proteins that incorporate metabolites and activate mitochondrial metabolism which triggers the differentiation into the stumpy form.
This is an irreversible switch.
How long after taking an infeced blood meal are procyclic trypomastigotes formed?
24-48 hrs.
What do procyclic trypomastigotes do? Where do they colonise?
Invade midgut through the PM and colonise the ectoperitrophic space.
After colonisaition by procyclic trypomastigotes, where do they go? What do they become here?
Go from the ectoperitrophic space through the oesophagus and colonise the salivary glands.
Once in salivary glands, they become infective metacyclics.
THey attach to epithelial cells in the salivary glands and detatch into saliva to be injected.
Why do metacyclics need to attach to salivary epithelial cells?
BEcause maturation to metacyclics takes several days but tsetses feed every other day. If not attached, they would be expelled before they are ready.
How long after an infected blood meal do we see infected salivary glands?
2 weeks to 30 days.
What other factors affect how likely a tryp infection is?
- sex and species- e.g. males tend to be better infected than females.
- if they are colony flies or from field due to different exposures to sialic acid which is required for parasitres (sialic acid enhances survival).
- ROS and complement responses/ immune system. e.g. toll pathway produces AMPs that form pores in parasites.
- Digestion- proteases, lipases etc affect parasites
- Temperature- behaviour e.g. shade seeking influences parasite development
- Microbiome e.g. wolbachia in gut. Tryps need correct microbiome to colonise
Describe the interaction between tsetse EP and T brucei procyclin
Procyclin on surface of parasites.
EP procides a protective role against parasites in midgut
EP is a specific immunoresponse protein.
Which two symtiont species dictate vectorial capacity? What are the locations of these?
Wigglesworthia and sodalis.
Wigglesworthis only in midgut. Sodalis all over fly.
How does tryp infection affect nutritional status and therefore fitness of fly?
Competes for proline in diet which is required for flight muscles. Therefore they can fly shorter distances when tryp infected.
How do tryps invade the ectoperitrophic space through the peritrophic matrix?
Do NOT breach/ go through it. Rather are incorporated through it as it forms in the place of PM synthesis.
DO all species of tryp have midgut cycles? Describe other events?
Mainly occurs with the T brucei group.
Vivax: stages only in mouthparts
Congolense: mix of both: has cycle in midgut but goes to mouthpart rather than salivary gland.
What does tryp express in the proventriculus, what for?
PSSA2.
KO unable to infect salivary glands. Needed for survival but not sure how or why.
What is the sialome?
catalogue of proteins expressed in the salivary glands.
Stuff like antigoagulants, anaesthetics etc.
How does infection impact the feeding of tsetses? What is the outcome of this?
means they take longer to feed as content of salivary proteins changed by tryps so thatthere is a change in clotting factors etc.
This interrupts feeding and makes it more likely the fly will take multiple incomplete blood meals from different hosts, thus increasing the opportunity for transmission.
What are serpins? Describe its structure: how is this useful?
Proteins preventing blood clotting and inhibiting the complement pathway. Upregulated in infection.
Similar structure to VSG but sticks out of the coating –> could be exploited as a vaccine target? Also because it does not recombine for an unlimited repertoire like VSG does.
