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.
How do ookinetes counteract the immune response?
Have a p47 protein on their surface which counteracts the complement-like response of the mosquito.
What is vectorial competence?
Vector competence is defined as “the ability of a vector to transmit a disease”. Ability to support development and transmission.
What is vectorial capacity?
Vectorial capacity is an equation of how many moquitos would be infected if biting a perfectly infectious person in one day.
What are the factors that reduce the efficiency of parasite infection?
- Bacteria in mosquito midgut
- Mosquito immunity
- Human complement in blood
What regulates/ activates transduction and modulation cascades in mosquitos against parasites? What is the result?
PAMPs of parasites are bound/ recognised by pattern recognition receptors or immune cells. Causes the production of NO (causes protein nitration) and ROS.
What is psf47?
A human malaria parasite gene that medaites the evasion of the immune response by malaria parasites. It suppresses the midgut nitration responses which are essential for activating the complement like systems. It determines vector compatibility with the parasite hence determining human transmission.
Why is it in the interest of the parasite to self regulate numbers?
Fewer parasites mean less of an immune response against them and reduced competition and increased vector survival (vector less likely to be overwhelmed and die).
What is melanisation?
The mosquito’s immune response against the parasites.
What are biotic non-genetic factors that influence infection possibility in a mosquito/ parasite development?
- Larval food competition
- Parental effect (state of mother may influnce infection of offspring?)
- Internal mosquito environment (e.g. other infection, microbiota)
What are abiotic non-genetic factors that influence infection possibility in a mosquito?
- Drugs in human blood
- Temp (thermal limits on parasites and vector)
- Insecticides
- Endectocides
- Mosquito diet
How does temperature affect the vector and parasite development?
Vector
- Bloodmeal digestion
- Larval development
- Adult survival
- Gonotrophic cycle
- Reproduction
- Immune responses
Parasite
-Sporogony aka extrinsic incubation period.
How do insecticides affect parasites?
Irrespective of mosquito insecticide resistance, insecticides can decrease parasite load / parasite prevalence.
How do endectocides affect parasites?
Inhibits sporogony.
How do drugs in human blood affect parasites?
- May influence mosquito microbiota and affect susceptibility as bacteria affect the immune system of the mosquito.
- Antiretroviral drugs affect gametocyte production and transmissibility
How does mosquito diet affect parasites?
What they eat affects the ability to transmit parasites.
- Males sugar feeding- digestion produces products which are toxic to parasites.
- Adult diet affects microbiota (affects parasite development)
What are attractive toxic sugar baits?
Baits using sugar to attract mosquitos for feeding. Include a toxic component that affects the parasite in the gut if it does not already kill the mosquito.
What is the significance of a normal blood meal on parasite development?
- Induces immune response (primed by the gut microbiota)
- Transmission blocking antibodies may be present in the blood e.g. psf48, 45 and 25
- Allocation of food to reproduction vs immune response balance.
What is the effect of Wolbachia presence on parasites?
Decreases the prevalence and intensity of sporozoites as it accelerates egg-laying (more energy diverted to this so parasites have less available energy). Wolbachia good, therefore, for parasite control.
What is the insect mechanism for metabolic resistance to insecticides? What are the effects of this on the vector and parasite?
Producing more P450 mono oxygenase enzymes which change the redox potential in cells.
Fitness cost to vector. Affects parasite development directly (may reduce the development of LF worms)
How do parasites change vector behaviour?
- Change in olfactory mediated behaviour to increase attraction to host (more human)
- Increase in persistence feeding and probing
- INcreases feeding when sporozoites are present but reduced when oocysts are developing
What are the physical costs to the vector of parasite infection?
- Physical damage of oocysts crossing midgut cells and sporozoites crossing salivary glands–> increases susceptibility to infection
- Fitness cost of energy diversion for parasite development.
