1. Apicomplexa originally called sporozoa no free-living forms
complex life cycles
spore-like forms
intracellular stages
defined by apical organelles
invasive stages
rhoptries
micronemes
gliding motility

2. Apicomplexa Infecting Humans
Plasmodium
Babesia
Toxoplasma
Sarcocystis
Isospora
Cryptosporidium
Cyclospora

3. Plasmodium causative agent of malaria ~155 named species
vertebrate hosts include: reptiles, birds, rodents, monkeys, and humans
specific for host
and vector
4 human species
no zoonoses or
animal reservoirs
transmitted by insect vector
Anopheles mosquito (mammalian)
P. falciparum
P. vivax
P. malariae
P. ovale

4. Life Cycle transmitted by mosquitoes sporozoites invade liver cells
exoerythrocytic schizogony (merozoites)
merozoites invade RBCs
repeated erythrocytic schizogony
gametocytes infective for mosquito
fusion of gametes in gut
sporogony on gut wall in hemocoel
sporozoites invade salivary glands

5. Transmission sporozoites injected with saliva enter circulation
trapped by liver (receptor-ligand)
Anopheles

6. Exoerythrocytic Schizogony
hepatocyte invasion
asexual replication
6-15 days
,000 merozoites
no overt pathology

7. Hyponozoite Forms relapse = hypnozoite recrudescence = subpatentt
only P. vivax and P. ovale
delayed replication (ie, dormant)
relapse = hypnozoite
recrudescence = subpatentt

8. meroite invasion can be broken down into 4 steps:
initial interaction: random (but in blood stream so immediate0 and probably reversible
the parasite then reorients so that the apical end is juxtaposed with the host membrane
a junction then forms between the parasite and host
parasite enters coming to lie within PV, but not a phagocytosis
presumaably the initial interaction involves the merozoite surface ….

9. Reorientation/Deformation.
a deformation of the erythrocyte is observed as the parasite reorients
the mechanisms of reorientation is not known
the reason though, obviously involve the location of the apical organelles at one end of the parasite
show rhoptry

10. Junction Formation
Entry

11. Erythrocytic Schizogony
intracellular parasite undergoes trophic phase
young trophozoite called ‘ring form’
ingests host hemoglobin
cytostome
food vacuole
hemozoin (malarial pigment)

12. Erythrocytic Schizogony
nuclear division = begin schizont stage
6-40 nuclei
budding merozoites = segmenter
erythrocyte rupture releases merozoites

13. erythrocytic schizogony
48 hr in Pf, Pv, Po
72 hr in Pm
gametocytes

14. Gametocytogenesis alternative to asexual replication
induction factors not known
drug treatment  #'s
immune response  #'s
ring  gametocyte
Pf : ~10 days
others: ~same as schizogony
sexual dimorphism
microgametocytes
macrogametocytes
no pathology
infective stage for mosquito

15. Gametogenesis occurs in mosquito gut ‘exflagellation’ most obvious
3X nuclear replication
8 microgametes formed
exposure to air induces
 temperature (2-3oC)
 pH (8-8.3)
result of  pCO2
gametoctye activating factor in mosquito
xanthurenic acid

16. Sporogony occurs in mosquito (9-21 d)
fusion of micro- and macrogametes
zygote  ookinete (~24 hr)
ookinete transverses gut epithelium ('trans-invasion')

17. Sporogony ookinete  oocyst asexual replication  sporozoites
between epithelium and basal lamina
asexual replication  sporozoites
sporozoites released

18. Sporogony sporozoites migrate through hemocoel
sporozoites 'invade' salivary glands

19. Invasive Stages
Merozoite
erythrocytes
Sporozoite
salivary glands
hepatocytes
Ookinete
epithelium