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Call of the wild diaries
Call of the Wild
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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. |
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| 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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