Describe various parasitic stages of Plasmodium falciparum............

Question

Describe various parasitic stages of Plasmodium falciparum and its molecular adaptations that help it escape the host immune response.

Answer 1

(a) P. falciparum infection in humans begins when an infected Anopheles sp. mosquito takes a blood meal and injects infective sporozoites into the peripheral circulation.

(b) Within minutes, these sporozoites invade hepatocytes in the liver and, over approximately one week, undergo asexual multiplication, producing tens of thousands of merozoite forms of the parasite.

(c) When the infected hepatocyte ruptures, merozoites are released into the peripheral circulation.

(d) The merozoites invade red blood cells (rbcs) and

(e) complete another round of multiplication within 48–72 h, with the production of 16–20 additional merozoites per rbc, which devour the rbc haemoglobin in the process.

(f) The released merozoites invade additional rbcs and carry on the cycle. It is the synchronous release of merozoites that is thought to be responsible for the periodic fevers associated with malaria.

(g) Some invading merozoites do not divide, but differentiate into male (microgametocyte) and female (macrogametocyte) sexual forms.

(h) These sexual forms are taken from the bloodstream by a feeding Anopheles sp. mosquito and

(i) fertilise in the mosquito midgut to form zygotes. These zygotes further differentiate into motile forms, called ookinetes, migrate through the mosquito gut wall and divide within oocysts on the external gut wall to form thousands of sporozoites.

(j) The infective sporozoites are released into the mosquito haemocoele and move to the salivary gland, where they await injection into another human host, thus completing the life cycle.

1.The parasites live inside cells, where they are largely hidden from the immune response.

2.Infection has a profound effect on the immune system including immune suppression. Dendritic cells suffer a maturation defect following interaction with infected erythrocytes and become unable to induce protective liver-stage immunity.