Question

Within the female Anopheles mosquito, the malaria-causing protist, Plasmodium sp., is in a gametocyte form, whereby the male gametocyte (microgamete) enters the female gametocyte (macrogamete) to form an ookinete that develops into an oocyst within the midgut of the mosquito. Within the oocyst, multiple sporozoites form, which upon rupturing of the oocyst the sporozoites are released and can infect humans when the female mosquito seeks out a blood meal and inoculates humans with their saliva.

Once entering the human bloodstream the Plasmodium undergoes two life cycle stages. The first is the exo-erythrocytic stage whereby the sporozoites enter hepatocytes and become schizonts that undergo asexual multiple divisions (hence their name). When the hepatocytes rupture merozoites are released and enter the bloodstream where they infect erythrocytes, which begins the second life cycle stage called the erythrocytic stage. Plasmodium uses erythrocyte surface antigens called Duffy factors to enter the cell. Upon entering the erythrocyte the merozoites become schizonts that fill the erythrocyte and eventually cause it to rupture and release more merozoites. These merozoites either re-infect erythrocytes or become gametocytes, which are taken up by Anopheles mosquitos when taking a blood meal.

While in erythrocytes, Plasmodium alters the surface proteins of the erythrocyte so that it will adhere to blood vessel walls, rather than pass through the spleen where infected erythrocytes are destroyed. Adhering erythrocytes occlude blood vessels and reduce blood flow, a conditioned called ischemia. Likewise, these adhering erythrocytes can pass Plasmodium through the blood vessel lining and into organs, which include passing through the blood-brain barrier and causing cerebral malaria.

a) What assumption can be made about Plasmodium’s ability to evade detection by the immune system? If detected, which Plasmodium life stages would be identified and why?

b) What cellular event marks the end of the exo-erythrocytis and erythrocytic stages? Will this event alter blood plasma cation concentrations? If yes, how and what (if any) would the repercussions be on neuronal potentials?

c) During ischemia, what type of metabolism is taking place in tissue deprived of oxygen? What metabolic by-product will accumulate in the tissue?

d) Systemic tissue cells have potassium/proton exchangers in their plasma membranes. What effect will this have on neuronal potentials?

Answer 1

Dear student,

a) Parasites replicate in the very rapidly in response to environmental pressures and they alter their structures in subtle ways to make themselves undetectable by the human immune system.

The sporozoites also invade the liver parenchymal cells very rapidly and adapt and goes undetected by the immune system.

b) exoerythrocytic cycle - In liver, the sporozoites becomes schizonts after repeated divisions and they burst releasing merozoites.

Erythrocytic cycle - The affected Erythrocytes bursts releasing merozoites. These merozoites can choose to infect new erythrocytes or they can develop into a gametocyte.

Calcium is needed for the growth of intraerythrocytic parasites and invasion of erythrocytes by the merozoites. So, extracellular calcium ions will be depleted.

c) During ischemia anaerobic metabolism occurs. The accumulated products are Co2, NADH, H+,Lactate, etc

d) Ca-ATPase exchange internal Ca++ for external H+.

Ca++-H+ exchange can account for extracellular pH changes which can occur by neuronal excitation.

Hope you are clear.