Malaria mosquito interactions Flashcards
How long after a gametocyte forms an ookinete does it penetrate the gut wall?
Takes 24 hours.
Which stage of parasite development takes the longest and is the most resource-intensive?
Ookinete.
What proportion of gametocytes form oocysts?
1%
What is the function of apyrase? How is this affected with malaria infection?
Prevents blood from clotting to keep bloodmeal flowing.
Is downregulated in malaria mosquitos so blood clots and interrupts feeding which causes more bprobing which increases the opportunity for transmission. Risk: risky as danger of squashing the more feeding there is.
What was thought to be the route of ookinetes vs what is actually the route? What occurs via this route/ what does this cause? What happens to these cells?
Thought to seek out specialised cells called Ross cells however they actually are thought now to go through the cells. Move laterally to neighbouring cells. These cells are induced into apoptosis and expelled from the other cells using a purse string mechanism.
Causes the induction of NO production via inducible NO synthase. Also inducible peroxidases.
How does NO production cause apoptosis?
Nitrite from NO reacts with peroxidase to form nitrogen dioxide. This causes protein nitration and subsequent cell death.
How does malaria affect egg production? Why?
Reduces mosquito’s fecundity and fertility (ability to produce offspring)
Does so because is energy intensive and reduces energy available for parasite.
What is vitellin? Where is it produced?
An egg yolk protein made of vitellogenin precursor which is produced in the fat body of the mosquito.
When does vitellin precursor expression peak?
12-36 hours after infection which is when ookinetes are forming.
What happens to vitellin when parasites are present throughout the first and second gonotrophic cycles?
Levels of vitellin are reduced in both cycles (reduces viability of eggs) when oocysts are present.
What happens to follicles when a mosquito is infected with malaria?
Increased follicle reabsorption = less eggs, at around the time when oocysts are invading the midgut.
This is also seen in tunnel assays where we can see that follicles and nurse cells are apoptosing meaning less egg development can be supported. (This induced apoptosis can be reduced by adding caspase inhibitors).
Why could cell death (e.g. infected midgut cells) benefit the mosquito?
- Increased mosquito fitness
- Reduced infection/ parasite burden
- More energy and resources for somatic processes.
What was seen when looking at egg number and number of parasites? Why? Why is it better for this to be a balance?
Positive correlation (opposite to what was previously thought). During egg production E20 hormone is produced which regulates egg production and has a side effect of increasing parasite numbers.
The balance between the number of parasites (therefore number of eggs) because fewer parasites (hence fewer eggs) causes faster sporozoite development, increasing chances of transmission in the field.
What is P falciparum’s non competitive strategy to maximuse transmission without incurring fitness costs to the mosquito?
It responds to reproductive investment by growing faster or more abundant.
How are ookinetes adapted to get through the midgut?
Express chitinase genes to break down the chitin component of the peritrophic matrix which acts as a physical barrier to prevent parasite penetration.
