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Mosquitoes & Malaria

Updated Thursday, 18 August 2016
In the Rough Science programme Call of the Wild, Rough Scientist Ellen has to develop a mosquito repellent

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Ellen

Zanzibar has a luxurious plant life and Ellen knows she can extract plant materials that will keep the mosquitoes at bay without making Kate smell too badly. However, the hard trick is proving the mosquito repellent works. Ellen will need to cover one of Kate’s arms with the repellent and leave the other arm clear, so she can show that only the arm without the repellent gets bitten. But that leaves another problem, mosquitoes carry diseases that they pick up from biting other people, so Ellen needs to raise mosquitoes from birth that haven’t bitten anybody yet and so will be disease free.

To find out more about the life cycle of the mosquito, read the following extract from the second level OU course Biology: Uniformity and Diversity (S204).

One of the most widespread infectious diseases of human beings is malaria, which kills more people than any other parasitic eukaryote, mainly in tropical countries. The agents which cause malaria are protoctists, Plasmodium spp. (phylum 11, Apicomplexa), whose life cycle provides a classic example in which there are several stages, each with a distinct morphology and function and is illustrated here.

Life cycle of a malarial parasite.

Life cycle of a malarial parasite Plasmodium vivax. Purple indicates haploid stages and pink diploid stages. RBC=red blood cells.

Notice that there are two hosts: human beings, where one stage of the life cycle occurs in liver cells and another in red blood cells; and a mosquito (Anopheles spp.). The mosquito picks up the parasite when it feeds on the blood of an infected person and transmits it in saliva after the parasite has passed from the gut to salivary glands.

 

Kate and Ellen

You can see that at stages A and B Plasmodium undergoes repeated cycles of asexual reproduction which can be viewed as subsidiary ‘loops’ on the overall cycle. Each stage in this complex life cycle has a different name. The notes below take you through the cycle step by step; you can also find out why malaria causes bouts of fever.

A–B Initial infection of a human host is by haploid cells (sporozoites) that migrate first to the liver. Within liver cells the sporozoites grow, undergo mitosis and produce many small amoeboid cells which are released when the liver cells rupture and may either infect another liver cell (an asexual loop) or infect red blood cells (erythrocytes). The role of the liver stage appears to be production of a Plasmodium cell with the capacity to infect red blood cells.
C

Within red blood cells, Plasmodium undergoes a cycle similar to that occurring in the liver, i.e. growth (a feeding stage), mitosis and release of small infective cells by rupture of the host cell. This stage is generally regarded as the main feeding and growth stage by the osmotrophic parasites. It is also the stage that causes greatest damage to human hosts and produces the characteristic symptoms of malaria. Not only are blood cells destroyed, there is also a release of parasite toxins from the ruptured blood cells which causes malarial fever. The infective cells infect more blood cells and this asexual loop may be repeated many times. Parasites are released synchronously from all infected blood cells which results in the bouts of fever typical of malaria.

The fever caused by Plasmodium vivax returns every second day whereas that caused by another species, P. malariae, does so every three days. The reason for this difference is that the generation time for growth, cell division and synchronous release of infective cells must be two days in P. vivax but three days in P. malariae.

D Eventually the infective cells differentiate into male and female gamonts (cells capable of producing gametes) which remain dormant within erythrocytes until sucked up by a mosquito, the secondary host.
E Once the gamonts have entered a mosquito stomach, the female gamont differentiates into a large, spherical female gamete (equivalent to an egg cell) and the male gamont divides to release many small, flagellated male gametes, which fuse with the female gametes to form zygotes. Each zygote becomes an elongated ookinete which bores through the wall of the mosquito’s stomach and becomes a thick-walled oocyst on the outside. Perhaps mosquitoes also feel ill at this stage.
F The oocyst nucleus now undergoes meiosis and the products—small, spindle-shaped cells—divide further by mitosis until they are eventually set free into the blood of the mosquito where they migrate to the salivary gland. The cycle then starts all over again.

Similar sorts of life cycle occur in many protoctist parasites and the complexity relates mainly to the problem faced by a parasite in transmitting from one host to another. Such parasites are highly specialized and their life cycles raise many questions.

 

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