Within the female Anopheles mosquito, themalaria-causing protist, Plasmodium sp., is in agametocyte form, whereby the male gametocyte (microgamete) entersthe female gametocyte (macrogamete) to form an ookinete thatdevelops into an oocyst within the midgut of the mosquito. Withinthe oocyst, multiple sporozoites form, which upon rupturing of theoocyst the sporozoites are released and can infect humans when thefemale mosquito seeks out a blood meal and inoculates humans withtheir saliva.
Once entering the human bloodstream the Plasmodiumundergoes two life cycle stages. The first is the exo-erythrocyticstage whereby the sporozoites enter hepatocytes and becomeschizonts that undergo asexual multiple divisions (hence theirname). When the hepatocytes rupture merozoites are released andenter the bloodstream where they infect erythrocytes, which beginsthe second life cycle stage called the erythrocytic stage.Plasmodium uses erythrocyte surface antigens called Duffy factorsto enter the cell. Upon entering the erythrocyte the merozoitesbecome schizonts that fill the erythrocyte and eventually cause itto rupture and release more merozoites. These merozoites eitherre-infect erythrocytes or become gametocytes, which are taken up byAnopheles mosquitos when taking a blood meal.
While in erythrocytes, Plasmodium alters the surfaceproteins of the erythrocyte so that it will adhere to blood vesselwalls, rather than pass through the spleen where infectederythrocytes are destroyed. Adhering erythrocytes occlude bloodvessels and reduce blood flow, a conditioned called ischemia.Likewise, these adhering erythrocytes can pass Plasmodiumthrough the blood vessel lining and into organs, which includepassing through the blood-brain barrier and causing cerebralmalaria.
a) What assumption can be made about Plasmodium’sability to evade detection by the immune system? If detected, whichPlasmodium life stages would be identified and why?
b) What cellular event marks the end of the exo-erythrocytis anderythrocytic stages? Will this event alter blood plasma cationconcentrations? If yes, how and what (if any) would therepercussions be on neuronal potentials?
c) During ischemia, what type of metabolism is taking place intissue deprived of oxygen? What metabolic by-product willaccumulate in the tissue?
d) Systemic tissue cells have potassium/proton exchangers intheir plasma membranes. What effect will this have on neuronalpotentials?
