Leishmania -sandfly interactions Flashcards
developmental strategies
Supraphylarian
periphylarian
hypopylarian
Suprapylarian development
Develop forward towards head region
eg. leishamania (leishmania) sp.
periphylarian development
behind the pylonis - go back, colonise the hindgut and then move forward into the mouthparts
eg. Vianna sp.
Hypophylarian development
Only go backwards - eg. leishmania (Sauroleshmaina) sp,
Parasite development
-Amastigotes
-procyclic promastigotes
nectomonad promastigotes
leptomonad promastigotes
haptomondad promastigotes
Metacyclics
Amastigotes
mammal infective form
no flagellum
kinetoplast is parallel with nucleus
ROLE - establish infection in sandfly
Procyclic promastigotes
Kinetoplast infront of nucleus nr. flagellar pocket
short stumpy flagella
Role - multiply in nutrient rich bloodmeal
nectomonad promastigotes
kinetoplat infront of nucleus
long falgellum
back end tapered to point
Attach to lectins of midgut by inserting flagellum btw, microvilli
Role - colonise sandfly and resist defecation and migrate from posterior to anterior gut
Leptomonad promastigotes
contracted form
multiply in thoracic and anterior midgut
Role - Secrete promastigote gel and block sandfly gut
haptomonad promastigotes
long thick flagellum
attach to cuticular lining of stomodeal valve by modified flagellum and hemidesmosome
Role - initiate biological plug for transmission
Metacyclic promastigotes
short slender body long flagellum
free moving and non dividing
accumulate in thoracic midgut and foregut
Role - infective stage - pre adapted for infection
How is metacyclic promastigote adapted for infection?
Modify LPG so can evade host cells
secrete more protease (gp63) involved in protecting from immune attack
immunologically silent - evade macrophages
Detach from midgut so free for transmission, able to move in gel
Barriers to successful development of parasite
- digestive ensymes
- lectins
- peritrophic matrix
- defecation
- attachment
- stomodeal valve
Digestive enzymes
midgut proteases peak 18-48 hrs after blood feeding
50-90% parasite killed in first 24hrs
parasites sensitive during amastigote - promastigote transformation - incomplete covering with LPG.
Lectins
bloodmeal increases 2-16 fold increase in lectin secretion
lectins can agglutinate parasites
inhibition of midgut lectin with sugars increases infection
Peritrophic matrix
parasites need to escape from PM
mesh of chitins, proteins and glycoproteins
sandfly degrades PM with chitinases before defecation
inhibition of chitinases led to increased losses of parasites
Defecation
second major loss of parasites
midgut peristalsis
promastigotes secrete microinhibitory peptide that can slow down midgut peristalisis
Attachment
LPG most abundant surface molecule phosphoglycan
2 forms of attachment
LPG mediated and non-LPG mediated
LPG mediated attachment
LPG deficient mutants cant attach
LPG -galectin attachment
metacyclogenesis is associated with changes to LPG
allows detachment of infective form from midgut
Non LPG mediated attachment
in non specific vectors attachment is LPG independant
Stomodeal valve
chitin lined one way valve separating the foregut and midgut
mature infection colonises and blocks the stomodeal valve
haptomonads - attach to chitinous wall
leptomondads- divide valve lumen and secrete gel
metacyclics - accumulate in blocked valve
Transmission from sandfly to host
2 main hypothesis
- innoculation from proboscis
- regurgitation from blocked stomodeal valve
PSG exacerbates infection
