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A Mutation Story, Essay Example

Pages: 2

Words: 627

Essay

In the early 1940’s, malaria caused exponential deaths and illness across Africa.  Even today there are approximately 655,000 deaths in Africa alone attributed to malaria and disease (McDaniel 2012).  While doctors were treating the patients that were stricken malaria they noticed a correlation between the survival rate of those suffering from malaria and the patients which had sickle cell anemia.  The real question is why a disease such as sickle cell anemia would produce a survival scenario for the patient whereas someone without sickle cell anemia would ultimately suffer from death.

Scientists and doctors studied this phenomenon to track down and try to understand the root cause of the survival so that the answer to the root cause could be made available as a potential solution for the rest of those impacted by malaria. Through investigation and research it was shown that since the genes which carried the sickle cell anemia disease would also have the potential increased survival rate to malaria (Packard, 2011).

Sickle cell anemia is a recessive disease but there is a higher concentration of carriers in Africa.  This concentration has led to a higher rate of survival against the plaguing malaria parasite that is widespread among the African population.  With sickle cell anemia, the blood cells are deformed from their original form which is why it is a negative aspect of having the disease but a potential benefit against malaria.

The populations of those that carry only part of the sickle cell disease do not suffer the extensive ramifications of the disease like those that carry a mutation on both sides of their cellular make-up.  The negative aspects of sickle cell anemia have an inverse positive gain against malaria.  The hemoglobin, which carries oxygen around the body, becomes distorted and warped during periods of strained and intense activity.  This warping of the hemoglobin causes a loss of oxygen.  The positive side is that the malaria parasite attaches to the sickle cells they also distort and warp.  Since they have a shift in shape and size parameters they are allowed to pass through the spleen.  The spleen removes the sickle cells along with the parasite (Nagel 2001).

With sickle cell anemia the hemoglobin cells run through the spleen and the spleen must work overtime to remove the proportionally larger quantity of misshaped and disfigured cells.  This could lead to splenic sequestration crisis in which the spleen is overworked and could lead to circulatory failure if not properly treated in a couple of hours (Bloom 1995).  The process that removes the parasites from the body is also the same process that if not attended to and treated could lead to death of the patient.

Prevention is the best form of treatment for malaria and this can be done by taking certain medications that the malaria parasite is still sensitive to.  There is also the thought and research around an immunization to the malaria strands but that is only feasible after repeated injections of the malaria strand.  This is not currently commercially available and not economically achievable outside of only the wealthiest countries (Bloom1995)

Integrating research into why sickle cell anemia and how the errors in DNA cause the malaria parasite to not be effective has led to many scientific breakthroughs regarding vaccination and prevention of the disease.  The paradigm between sickle cell anemia and its horrific end state and its potentially lifesaving hemoglobin alterations that negate the impact of malaria is as intriguing today as it was in the 1940’s.

References

Bloom, M. (1995). Understanding sickle cell disease. Jackson: University Press of Mississippi.

Nagel, R., (2001). “A mutation story”. WGBH Educational Foundation and Clear Blue Sky Productions.

McDaniel, K., (212). “NetsforLife: malaria statistics”. Retrieved from http://www.netsforlifeafrica.org/malaria/malaria-statistics

Packard, R. (2011). The making of a tropical disease: a short history of malaria. Baltimore: The Johns Hopkins University Press.

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