These lecture notes are the forth in a series from the module biodiversity: exploiters and exploited. This lecture covers everything about malaria from its impact, to transmission via mosquitos and how we tackle it. A great way to start your understanding in this module (or help you get out of the ...
Lecture:
Claims 1mil lives
Parasite (Plasmodium) – Protozoan (Euk)
Members of phylum = all intracellular parasites
o Main – P. vivax (Europe), P. falciparum (90% deaths – not well adapted to humans
so always kills instead of keeping hosts), P. ovale and P. malariaae (rare), P. knowlesi
(monkey malaria – evolving to human
malaria)
o Lifecycle:
10 lifecycle phases
In mosquito (sexual repo)
Replication 1 – amplification
(mitosis)
Gametocytes
o Macrogametocytes =
female (not broken
down)
o Microgametocytes = male (not broken down by mosquito)
o Ingested and egg/sperm fuse in mosquito gut to form zygote
Diploid zygote performs meiosis to form haploid
ookinete cells
The cells form oocysts (seen on EM) – amplification
Cyst bursts to release sporozoites and then they
travel to salivary glands (w/anaesthetic) to pass
onto next host
Sporozoite injected by mosquito -blood/lymphatics→ liver
Merozoites and RBCs broken down
Takes 2 weeks for readministration/reinfection of mosquito (gets
colder = stops)
In human liver
Replication 2 – amplification (merozoites released to RBCs)
Sporozoite becomes a less invasive hepatic trophozoite cell
Sporozoite’s infect cell to become a hepatic schizont cell
Merozoites (1.2um) released into blood
o P. vivax and P. ovale have resting periods in liver as
hypnozoites
In human RBC
Amplification in RBC
Merozoite becomes trophozoite or gametocytes (ingested→repo)
Merozoites make pocket in RBC and feed on Hb in RBC
Granules on outside of RBCs = falciparum waste
Gets cells stuck in caps so that not consumed by liver
, 22.10.19
16 new merozoites in RBC and bursts
Infection builds up (synchronized bursting = fevers)
o Staining RBCs show merozoites stages in the RBC
Mosquito (Anopheles)
o Female (suck blood), Anopheles genus = transmitting vector
5 bites required to ensure infection
o Lifecycle
Blood meal from host to rear batches of eggs
Rest and digest meal to mature eggs
Lays 50-150 eggs in water and hatch in 2-3 days
Larval stages in top of water (at an angle flat to surface)
Pupates in water with breathing tube
Leaves water when adult (3 days after hatching)
o Unknown how many species (morph similar but behaviour/requirements different)
Malaria effects
o 2018
435,000 deaths/year (61% < 5 years old bc ↓ innate immunity)
Young adult in malaria area = infect/survive bc repeated infection
o Lost immunity by leaving malaria area/when pregnant
3.4 billion people at risk of malaria
Malaria symptoms
o After synchronised bursting of RBCs
o Stage 1 = headache, cold, shivering
o Stage 2 (1 hour later) = 41֯C w/↑ sweating
o Stage 3 (8-9 hours later) = normal temp but exhausted
o P vivax and P. ovale = cyclical fever 1 day of fever and 3 days off
P vivax = anaemia, lung issues and rarely coma
↑∆ relapse bc fast production of sporozoites in mosquitoes at low
temps
o P. malariae = quartan fever 1 day on and 1 day off
Causes kidney disease (occurs decades later if in resting phase)
o P. falcipaeum = cyclical fever w/ coma, fits and death
Bc ↑# of infected RBCs
Sequestration
Endemic to Saharan Africa (natural immunity – breast milk?)
Natural immunity for being infected for 10-15 years 5x/year
Immunosuppression in preg = ↑ susceptibility
Malaria control
o Move out of malaria areas (low-lying areas/Southern lowlands were infected in
summer, two house – one for winter too)
o Quinine
Bark of cinchona tree
South America/Andes (high humidity and altitude)
Discovered in 1632 (locals used beforehand)
Reduce symptoms and kill blood stage of bacterium
Europeans introduced malaria as not native to SA looking for malaria cure
Dried samples sent back and ground up bark = Jesuit’s powder
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