The parasites that cause malaria usually enter a person’s body after a female anopheles mosquito has bitten them. The parasite contained in the female anopheles mosquito enters the body through the bloodstream and goes to the liver (Eleonore et al., 2020). It is from the liver that the parasite matures. After it has matured enough, the parasite leaves the liver and goes ahead to infect the red blood cells. Malaria is caused in the body by a single-celled parasite (Archer et al., 2018). That single-celled parasite comes from the genus Plasmodium. Only female anopheles mosquitoes carry the malaria parasite, and they must feed from the blood of an individual with malaria to carry the parasite. People with sickle cell disease cannot get malaria since it is an adaptive response against malaria. The sickle cells have membranes that usually stretch to abnormal shapes (Archer et al., 2018). The cells usually become porous with time and leak the nutrients the malaria parasites need for survival. After the abnormal cells have been destroyed, the parasite is also destroyed along with them (Archer et al., 2018). That is why it becomes difficult for people with sickle cell disease to get malaria.
The evolutionary link associated with the sickle-cell trait indicates that humans can adapt. Humans adapted to the resistance between sickle-cell trait and malaria resistance. The gene mutation that caused sickle cell disease originated in areas where malaria was prevalent (Sundd et al., 2019). Such areas included Africa, Asia, and the Middle East. These cells appeared and went extinct several times to the point where permanency was established. The permanency was established after a notorious form of malaria moved from animals and entered the body of humans (Eleonore et al., 2020). That led to the creation of the sickle-cell disease that was malaria resistant. That communicates why people in malaria prevalent areas can remain productive despite their environmental conditions. The mutation that occurs in the beta-globin chain of the hemoglobin molecule is the one that leads to sickle cell disease. That goes ahead to create sickle cell hemoglobin. The sickle cell hemoglobin adapts the characteristic of polymerizing when deoxygenated (Sundd et al., 2019). That leads to the destruction of the normal shape of the red blood cells. It also increases the chances of the red blood cells being deformed. That is how sickle cell disease adapts to the body.
Many people who no longer live in parts of the world where malaria is prevalent still develop sickle cell disease due to increased migration. The movement of people to areas where malaria does not exist causes people from those countries to also get the disease (Honsel et al., 2019). Sickle cells can also be transmitted genetically. That means that the moment sickle-celled people from Sub-Saharan Africa move to Europe and America, there is a high chance that they will spread the diseases to other people if they intermarry (Honsel et al., 2019). The increased life expectancy of the patients from malaria-infested regions makes sickle cell diseases highly prevalent. Most sickle cell disease cases reported in areas that do not have malaria arise from inheritance.
The best advice to give families with sickle cell disease cases is to get all the required vaccinations. They need to ensure that they take their kids to all the vaccinations to protect their immune systems (Archer et al., 2018). There is a need to go for the flu, pneumococcal, and coronavirus vaccines. Going for folic acid supplements is also required so the kids can help make new red blood cells. That will help in making up for the destroyed ones. The families also need to ensure that they get enough exercise and take medicines to help manage pain (Archer et al., 2018). That will help the sickle cell victims to live healthy lives.
References
Archer, N. M., Petersen, N., Clark, M. A., Buckee, C. O., Childs, L. M., & Duraisingh, M. T. (2018). Resistance to Plasmodium falciparum in sickle cell trait erythrocytes is driven by oxygen-dependent growth inhibition. Proceedings of the National Academy of Sciences, 115(28), 7350-7355. https://www.pnas.org/doi/10.1073/pnas.1804388115
Eleonore, N. L. E., Cumber, S. N., Charlotte, E. E., Lucas, E. E., Edgar, M. M. L., Nkfusai, C. N., … & Mbanya, D. (2020). Malaria in patients with sickle cell anemia: burden, risk factors and outcome at the Laquintinie hospital, Cameroon. BMC infectious diseases, 20(1), 1-8. https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-019-4757-x
Honsel, V., Khimoud, D., Ranque, B., Offredo, L., Joseph, L., Pouchot, J., & Arlet, J. B. (2019). Comparison between adult patients with sickle cell disease of sub-Saharan African origin born in metropolitan France and sub-Saharan Africa. Journal of clinical medicine, 8(12), 2173. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6947353/
Sundd, P., Gladwin, M. T., & Novelli, E. M. (2019). Pathophysiology of sickle cell disease. Annual review of pathology, pp. 14, 263. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053558/
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