Read this article to learn about Life Cycle of Plasmodium in Mosquito !
Malaria is one of the most widely known diseases since time immemorial. It is caused by a pathogenic protozoan of blood, Plasmodium.
Four species of Plasmodium, viz., P. vivax, P. falciparum, P. malariae and P. ovale are so far known to infect human beings causing different types of malaria. Female Anopheles mosquito serves as the carrier or vector hosts and transmits plasmodium from person to person. Plasmodium is an intracellular parasite in RBCs of man.
It is also reported from birds, reptiles and various mammals. Plasmodium is widely distributed in tropical and temperate countries the world over. Plasmodium vivax requires two hosts to complete its life cycle- a primary or definite host and a secondary or intermediate host. Such a two host life cycle is digenetic. Intermediate host is female Anopheles. In human body the parasite multiplies asexually while in female anopheles it undergoes a sexual cycle followed by an asexual multiplication called sporogony.
Asexual cycle in man:
The normal adult or trophozoite phase of plasmodium occurs in RBCs of human beings. The parasite first invades the liver cells for asexual multiplication.
The life cycle of plasmodium in man is can be studied under the following heads:
(i) Exoerythrocytic cycle:
When an Anopheles mosquito bites a human to suck blood. Plasmodium is inoculated into human blood in the form of a minute infective stage called Sporozoites (fig. 9.3). The injected sporozoites invade the hepatocyte cells in the liver. In the liver cell, a sporozoite actively feeds on its cytoplasm and grows into a large (about 45 in diameter) and spherical adult like form called cryptozoite.
This form multiply into thousands of cryptomerozoites by multiple fission called schizogony (exoerythrocytic schizogony). In such a multiplication repeated nuclear divisions first result into multinucleate organism, and then divides by cytoplasmic segregation around the tiny daughter nuclei. Due to the pressure of cryptomerozoites, the body of cryptozoites as well as the host liver cell ruptures liberating the cryptomerozoites into liver sinusoids. Some of these invade fresh liver cells to continue exo-erythrocytic schizogony, while others remain in blood sream and invade erythrocytes (RBC) to initiate erythrocytic cycle.
(ii) Erythrocyic cycle:
This cycle takes place in RBCs after the RBCs are invaded by cryptomeromerozoites. After invading an erythrocyte, a cryptomeromerozoite soon becomes a rounded, disc like structure called trophozoites (fig. 9.4). As it grows, a contractile vacuole appears in its centre, pushing the cytoplasm and nucleus to a thin peripheral layer and the parasite attains a ring Ike appearance to represent the signet ring stage.
After some time, the vacuole disappears and the parasite assumes an amoeboid shape. The trophzoites actively feed upon the haemoglobin of RBCs and increases in size till the entire corpuscle gets filled with it. This forms the schizont stage and its cytoplasm contain yellowish-brown pigment granules, the haemozoin. It is formed by the decomposition of haemoglobin. The schizont undergoes asexual multiplication termed as schizogony or merogony.
(iii) Schizogony or merogony:
The nucleus or the schizont divides by multiple fission to from 6-24 daughter nuclei which migrate towards the periphery. After some time the totally exhausted erythrocyte bursts liberating the merozoites and the toxic waste (haemozoin granules) into the plasma of blood. These attack the fresh R.B. Cs. And repeat the erythrocytic schozogony. One erythrocytic cycle is completed within 48-72 hours.
As the parasite continues to destroy the R.B.Cs. of the host, the host becomes anemic and its toxin accumulates in the plasma. After about 5 successive erythrocytic cycles the malarial symptoms develop for the first time and the host suffers from paroxysm of chill and fever which are now repeated at the end of each schizogony. Thus the parasite passes a latent period of about 10 to 15 days since its inoculation in the body of host. This period is known as incubation period.
(iv) Formation of gametocytes:
As a result of repeated schizogony in the blood stream, the parasite becomes so potential that its existence is threatened due to lack of fresh R.B.Cs. and the resistance of the host. Consequently, the parasite prepares to enter the new host by the formation of gametocytes. Some of the meozoites, after entering the R.B.Cs. neither form trophozoites nor multiply by binary fission but grow slowly and become compact bodies, the gametocytes. These are of two types:
The more numerous, but small in size and with a large centrally placed nucleus, are the microgametocytes, potentially male. The less numerous but larger in size and with a greater amount of dense cytoplasm and a small nucleus are the macro or mega gametocytes, potentially female. The mature gametocytes are unable to develop further in the body of primary host and can survive only for two days. They reach the superficial blood vessels and wait for the bite of female Anopheles.
Sexual Life-Cycle in Anopheles:
When Anopheles sucks the blood of a diseased man, the parasite under different stages of development enters its alimentary canal. But only the gametocytes are able to survive, while others are digested. The gametocytes are set free by the rupture of R.B.Cs. and develop further to form gametes.
(i) Development of male gametes:
The nucleus of microgametocyte divides repeatedly to form 6 to 8 haploid nuclei, as one of these divisions is a reduction division. Each nucleus is surrounded by a little of cytoplasm and metamorphoses into a male gamete. Each has a small body with a nucleus and a cytoplasmic flagellum. By the lashing movement of their flagella the male gametes swim in the stomach fluid.
(ii) Development of female gametes or microgamete’s:
The nucleus of the macrogametocyte undergoes reduction divisions forming two nuclei. One of them protrudes out as a polar body and the other comes to lie in a protuberance which is known as reception cone. Thus the macrogamete is formed.
(iii) Syngamy or fertilization:
The actively moving male gamete is attracted by the macrogamete and penetrates it through the reception cone. The nuclei of the two fuses together forming the synkaryon. Syngamy is anisogamous and the zygote thus formed is inert and round.
Soon the rounded zygote elongates and assumes the vermiform appearance and becomes motile. It is now known as vermicule or ookinete (fig. 9.5). Its anterior en4 is pointed and with this it penetrates the stomach wall to come to lie in the sub-epithelial tissue underneath the outer limiting membrane. It becomes rounded, secretes a thin membranous cyst and is known as sporont or oocysty. It feeds by absorption and increases in size.
The nucleolus of the fully mature oocyst undergoes multiple fission by mitosis producing a large number of daughter nuclei. These get surrounded by fragments of cytoplasm. The irregular uni-nucleate bodies thus formed are known as sporoblasts. The nucleus in each sporoblast divides repeatedly by mitosis.
The nuclei form spindle-shaped sporozoites. These are liberated in the haemocoel or body cavity by the repture of cyst wall. The sporozoites now move to different body organs and also the salivary gland (fig. 9.6). With the entrance of parasite in the salivary glands the female Anopheles becomes infective and is able to inoculate the parasite into the blood-stream of healthy persons.
Control of Malaria:
All measures of control of malaria are divided under the following three categories:
(i) Elimination or destruction of vector, i.e., Anopheles mosquito.
(ii) Prophylaxis, i.e., prevention of infection.
(iii) Treatment of the infected patient.