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In-Depth Information
A few symptoms of sickle cell anemia are joint pain, fatigue, breathlessness, delayed
growth, jaundice, abdominal pain, and susceptibility to infections.
Hemolytic crisis, sequestration crisis, and aplastic crisis are three different types
of episodes. Hemolytic crisis is a result of damaged red blood cells that break down
and is one of many life-threatening consequences of having sickle cell anemia.
Sequestration crisis is due to the spleen enlarging and trapping the blood cells.
Aplastic crisis is an infection that causes the bone marrow to stop producing red
blood cells. Without proper medical attention, individuals with this disease often
die at an early age.
Although no cure exists for this disease, a few steps can be taken to help prevent
people from inheriting sickle cell anemia in the future. Prenatal diagnosis of sickle
cell anemia and genetic counseling are available. As for the future fight against
this disease, improvements continue to be made, and as the medical community
continues to advance so will the health and lives of those with sickle cell anemia.
People with the sickle cell trait, a genetic condition, are not as easily infected
with malaria. Heterozygous individuals having no or slight sickle cell anemia are
more resistant to malaria because the parasite is unable to grow in red blood cells
with sickle cell hemoglobin.
The following model mimics the balance between sickle cell anemia and malaria
in developing African countries. We will use this model to explore the effects of
antimalaria drugs and medical treatment on the frequency of sickle cell anemia.
Specifically, the model focuses on the genetic balancing act between sickle cell ane-
mia in a representative African population that has no immigration or emigration.
Malaria infection is assumed to be largely endemic.
Infectious disease population model components are set up individually for the
three possible genotypes (AA, AS, or SS), with susceptible (SUSC), infectious
(INF), and immune stocks for each (Figures 4.9-4.11). The rate of infection is de-
pendent on the number of susceptibles in the particular genotype, the total number
of infectious individuals following a lag due to a latent period (A DELAY), and a
transmission coefficient (Trans), which is a function of a transmission rate (TR) and
the level of infected vectors.
The level of infected vectors is complex and could be modeled separately, but
since we are modeling an endemically infected population, this parameter is simpli-
fied by providing only seasonal variability and a degree of randomness. The AS and
SS genotypes have a lower transmission rate TR than the AA genotype since these
individuals have partial resistance to malaria, unlike the AA individuals.
All of the stocks have a death rate associated with them. Most have a natural death
rate, while the infectious stocks have a higher death rate due to malaria. Also, the
SS genotype stocks have an additional death rate due to sickle cell anemia (Anemia
DR). Individuals recover at a certain rate, and immunity is lost at a certain rate.
The total number of each genotype and allele, as well as the frequencies of each,
are calculated in the genetic portion of the model (Figure 4.12). The allelic frequen-
cies at each time step are used to determine the genotype of individuals born into the
population and therefore which of the three diseased population models individuals
will enter.
