Leishmania - sandfly interactions Flashcards
What are the three different developmental strategies of leishmania?
Hypopylarian, suprapylarian and peripylarian
Name each stage in the leishmania developmental cycle
Amastigote, procyclics, nectomonads, leptomonads, haptomonads, metacyclics.
What is the role of the amastigote form?
To establish infection in the sandfly, entering in the blood meal.
What is the role of the procyclic form?
To multiply in the nutrient rich blood meal.
Where does the nectomonad form attach?
It attaches to the lectins of the midgut by inserting the flagellum into the microvilli to colonise the gut.
What is the role of the leptomonad form?
To secrete the promastigote gel and block the anterior midgut ready for transmission.
Where does the haptomonad attach?
To the cuticular lining of the stomedeal valve that separates the midgut from the foregut, forming a plug with the gel.
Which form of the leishmania cycle is infectious in vertebrate?
Metacyclics - final form of development.
How are the metacyclics pre-adapted for infection?
Free moving in the gel and no longer can reattach to midgut.
They are immunogenically silent to evade macrophage.
They produce proteases to protect from complement.
LPG enables efficient cell invasion.
How are digestive enzymes a barrier to successful parasite development?
Midgut proteases peak 18-48 hours after the blood feed and kill 50-90% of parasites during this phase.
What is the role of lectins in controlling parasite infection in the sandfly?
Lectins agglutinate the parasite - cross link LPG, to reduce infection establishment.
How does the leishmania parasite overcome the peritrophic matrix?
Uses its chitinases to degrade the matrix to escape/migrate through the PM.
How does the parasite avoid being lost during the defecation phase after the bloodmeal?
It secrete myoinhibitory peptides that slow or paralyse peristalsis to delay defecation.
How can high expression of leishmania chitinases result in more parasite transmission per sandfly bite?
Chitinase over expression leads to early colonisation of the stomedeal valve, and more damage to the valve. This results in the fly having to feed for longer so more parasites are delivered per bite.
Give two main hypotheses as to how the parasite is transmitted from the sandfly?
Inoculation of the proboscis, or regurgitation from blocked stomedeal valve where it will take time for the fly to push the blood through the blockage.
