Leishmania -sandfly interactions

Question 1

developmental strategies

Answer 1

Supraphylarian
periphylarian
hypopylarian

Question 2

Suprapylarian development

Answer 2

Develop forward towards head region

eg. leishamania (leishmania) sp.

Question 3

periphylarian development

Answer 3

behind the pylonis - go back, colonise the hindgut and then move forward into the mouthparts
eg. Vianna sp.

Question 4

Hypophylarian development

Answer 4

Only go backwards - eg. leishmania (Sauroleshmaina) sp,

Question 5

Parasite development

Answer 5

-Amastigotes
-procyclic promastigotes
nectomonad promastigotes
leptomonad promastigotes
haptomondad promastigotes
Metacyclics

Question 6

Amastigotes

Answer 6

mammal infective form
no flagellum
kinetoplast is parallel with nucleus
ROLE - establish infection in sandfly

Question 7

Procyclic promastigotes

Answer 7

Kinetoplast infront of nucleus nr. flagellar pocket
short stumpy flagella
Role - multiply in nutrient rich bloodmeal

Question 8

nectomonad promastigotes

Answer 8

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

Question 9

Leptomonad promastigotes

Answer 9

contracted form
multiply in thoracic and anterior midgut
Role - Secrete promastigote gel and block sandfly gut

Question 10

haptomonad promastigotes

Answer 10

long thick flagellum
attach to cuticular lining of stomodeal valve by modified flagellum and hemidesmosome
Role - initiate biological plug for transmission

Question 11

Metacyclic promastigotes

Answer 11

short slender body long flagellum
free moving and non dividing
accumulate in thoracic midgut and foregut
Role - infective stage - pre adapted for infection

Question 12

How is metacyclic promastigote adapted for infection?

Answer 12

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

Question 13

Barriers to successful development of parasite

Answer 13

• digestive ensymes
• lectins
• peritrophic matrix
• defecation
• attachment
• stomodeal valve

Question 14

Digestive enzymes

Answer 14

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.

Question 15

Lectins

Answer 15

bloodmeal increases 2-16 fold increase in lectin secretion
lectins can agglutinate parasites
inhibition of midgut lectin with sugars increases infection

Question 16

Peritrophic matrix

Answer 16

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

Question 17

Defecation

Answer 17

second major loss of parasites
midgut peristalsis
promastigotes secrete microinhibitory peptide that can slow down midgut peristalisis

Question 18

Attachment

Answer 18

LPG most abundant surface molecule phosphoglycan
2 forms of attachment
LPG mediated and non-LPG mediated

Question 19

LPG mediated attachment

Answer 19

LPG deficient mutants cant attach
LPG -galectin attachment
metacyclogenesis is associated with changes to LPG
allows detachment of infective form from midgut

Question 20

Non LPG mediated attachment

Answer 20

in non specific vectors attachment is LPG independant

Question 21

Stomodeal valve

Answer 21

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

Question 22

Transmission from sandfly to host

Answer 22

2 main hypothesis

• innoculation from proboscis
• regurgitation from blocked stomodeal valve
  PSG exacerbates infection