NATIONAL CENTER FOR CASE STUDY TEACHING IN SCIENCE

African Illness: A Case of Parasites?

by
Kevin M. Bonney
Cohen School for Human Services and Education
Metropolitan College of New York, NY

Part I – Sub-Saharan Safari

A 51-year-old man named Robert Bragg reported to a hospital in the United Kingdom complaining of general malaise
(discomfort), myalgia (muscle pain), fevers, headache, vomiting, and diarrhea. He complained that during the day he
felt weak and tired; he was unsure if this was because his symptoms kept him awake at night, or if something else was
causing his fatigue.

Robert had recently returned from a two-week safari in central Africa. He said that he felt fine during the entire
trip, but reported that he had received numerous bug bites while on safari. He also said that while he was in Africa
he routinely ate unfamiliar foods, including meats, which may have been prepared and stored under conditions that
would not be considered sanitary practices in the United Kingdom.

Doctors suspected Robert’s symptoms were caused by an infection he developed while on safari.

Questions
1. Make a list of human pathogens that are endemic to sub-Saharan Africa and can be transmitted through bug
bites or consumption of contaminated foods. Looking over your list, what do you think is the most likely
cause(s) of Robert’s illness?
2. What tests should doctors conduct to confirm this diagnosis?

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Part II – Diagnosis
Because Robert had spent much of his time outdoors in an area of the world where the Anopheles mosquitoes that
transmit malaria are common, the doctors immediately suspected he had contracted malaria. His symptoms matched
those generally expected of people with malaria, but to confirm the diagnosis doctors collected a blood sample from
Robert to analyze for the presence of the Plasmodium falciparum parasites that cause the disease.

When doctors looked at Robert’s blood smear under a

Figure 1. T. brucei trypomastigotes (blood stage form) in a blood smear.
light microscope, they did not see any malaria parasites.
However, they did make a startling discovery.

“I found Trypanosoma brucei parasites in the patient’s

blood,” one of the doctors remarked.

“What is Trypanosoma brucei? ” asked a nurse. “Is it a

type of malaria?”

“Trypanosoma brucei is a protozoan parasite. It is not

closely related to Plasmodium falciparum genetically,
but there are many similarities in the way it infects
people and in the symptoms it causes. The disease
caused by Trypanosoma brucei, called African
trypanosomiasis, is also known as African sleeping Image courtesy of Centers for Disease Control and Prevention/ Dr.
sickness. All of the patient’s symptoms are explained Mae Melvin, ID# 10167 in CDC Public Health Image Library
(PHIL). Public domain.
by this diagnosis.”

Use the sources below to learn more about African trypanosomiasis.

• “Parasites—African Trypanosomiasis,” Centers for Disease Control and Prevention

http://www.cdc.gov/parasites/sleepingsickness/

• “Trypanosomiasis, African,” World Health Organization (WHO)

http://www.who.int/topics/trypanosomiasis_african/en/

After thoroughly investigating these and other relevant sources, answer the questions below.

Questions
1. What is a protozoan? How is a protozoan parasite different from bacteria and multi-celled parasites such
as intestinal worms? How does T. brucei differ from the closely related American trypanosome T. cruzi, the
causative agent of Chagas disease, and from the P. falciparum parasite that causes malaria? Describe notable
differences in morphology, life cycle, infectivity, transmission, geographical range, disease presentation, and
treatment.
2. How do people become infected with T. brucei? What are the risk factors as far as behavior, lifestyle, and
geographic location?
3. What are the clinical manifestations and symptoms of African trypanosomiasis? Compare and contrast these
with the symptoms of malaria.
4. Why does T. brucei infection cause the symptoms that led to the term “African Sleeping Sickness”?
5. How is T. brucei infection diagnosed? What factors often make diagnosis difficult?

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Part III – Symptoms and Treatment

The doctors informed Robert of the diagnosis. After they explained the cause of his illness, Robert asked “Will I be ok?
Do you have a medication to kill Trypanosoma brucei?”

“There is medication to treat this disease, Mr. Bragg,” said the doctor. “It’s called suramin. It is very effective at killing
Trypanosoma brucei when given early enough in the disease process, but it can also cause severe side effects, including
joint pain, severe weakness, light sensitivity and even loss of consciousness. We need to start your treatment at once
despite these side effects because the disease has a high fatality rate if left untreated. Fortunately, you are not exhibiting
signs of severe damage to your central nervous system, such as violent behavior, convulsions, or coma, so I think that
we have caught the disease at an early enough stage for treatment to be successful. However, we will first examine your
central nervous system (CNS) fluid for the presence of parasites to confirm that the disease has not progressed.”

“All right, doctor. Do what you have to… but is there any chance that I can recover from this parasite on my own,
without risking the side effects of that medication?”

A second doctor interjected: “Actually, the human immune system is somewhat capable of killing Trypanosoma
brucei and lowering the parasitemia (number of parasites in the blood); however, the parasite has adapted a way to
continually evade the immune system so that it can continue replicating.”

“If we were to count the number of parasites in your Figure 2. Parasitemia level vs. time
blood every day,” explained the doctor, “we would
likely notice that the parasitemia level would steadily
Number of parasites

increase for a period of time, perhaps one week, then

the parasitemia level would fall drastically over one or
per ml of blood

two days as large numbers of parasites were killed by

your immune system, only to rise again the following
week. This trend would continue until you were given
medication to clear the parasites, and would look like
this if graphed.” The doctor then pointed to a graph in
Time
a paper he was holding (Figure 2).

“I don’t understand,” said Robert. “If my immune system is capable of killing the parasites, why would the number of
parasites in my blood repeatedly rebound in that way?”

The doctor explained that in order for African trypanosomes to become successful extracellular parasites and survive in
the bloodstream of their human hosts, they had evolved a mechanism to evade the host’s immune response.

“African trypanosomes are covered by a protective coat containing proteins called variant surface glycoprotein
(VSG). Although VSG helps protect the parasite, it’s also an antigen, which means it triggers the immune system to
respond by making antibodies against it, which can lead to the destruction of the parasite. The genome of African
trypanosomes contains many variations, or alleles, of the gene that encodes VSG. Only one allele is expressed at a time,
but the parasite can vary which allele is expressed, allowing it to change its VSG coating as soon as the host’s immune
system becomes effective at recognizing one particular variant of VSG.”

The doctor continued: “Every spike in parasitemia levels in the graph represents a switch in VSG expression. It takes
time for the immune system to adapt to each new VSG. Once it does, parasites are rapidly killed and parasitemia
levels drop sharply, only to increase again after another round of VSG switching.”

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Questions
1. Investigate the different parts of the human immune system and explain which cells/products of innate and
adaptive immunity are responsible for recognizing antigens on the surface of T. brucei and clearing the parasite.
2. What would happen if T. brucei suddenly loss the ability to undergo antigenic variation?
3. If researchers developed a drug that could prevent T. brucei from undergoing antigenic variation, do you think it
could be successful in eradicating African Sleeping Sickness? Would the drug have to be administered at a certain
point before or after infection in order to be helpful?
4. Based on the similarities and differences you identified earlier between T. brucei, P. falciparum, and T. cruzi, do
you predict that P. falciparum and T. cruzi undergo similar antigenic variation? Why or why not?

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Part IV – Public Health Campaign

In addition to the extensive toll on human life, African trypanosomes also cause a widespread and devastating disease
in livestock cattle called Nagana. Nagana causes three million cattle deaths per year, which amount to a loss of $4
billion a year to struggling African economies. Because there is no effective vaccine against African trypanosomes, the
most effective way to prevent the spread of the disease is through multi-faceted public health campaigns directed at
eliminating parasite contact through other means.

Design a public health campaign to dramatically reduce or eradicate African trypanosomiasis in both humans and
cattle from a community in Africa. In your plan, include strategies to stop the spread of African trypanosomes, as well
as ways to educate the public and local governmental and health agencies so that this information can be disseminated
and implemented.

References
Internet Sites
Parasites—African Trypanosomiasis, Centers for Disease Control and Prevention (CDC).
http://www.cdc.gov/parasites/sleepingsickness/
Trypanosomiasis, African, World Health Organization (WHO).
http://www.who.int/topics/trypanosomiasis_african/en/
Stamp Out Sleeping Sickness.
http://www.stampoutsleepingsickness.com/home.aspx
Image of T. brucei trypomastigotes, image ID #10167, from Centers for Disease Control and Prevention (CDC).
http://phil.cdc.gov/PHIL_Images/10167/10167_lores.jpg
Suramin, Mayo Clinic.
http://www.mayoclinic.com/health/drug-information/DR601283/DSECTION=side-effects
African Trypanosomiasis or Sleeping Sickness, Public Health Agency of Canada.
http://www.phac-aspc.gc.ca/tmp-pmv/info/af_trypan-eng.php

Journal Articles
Horn, D., and R. McCulloch. 2010. Molecular mechanisms underlying the control of antigenic variation in African
trypanosomes. Current Opinion in Microbiology 13(6): 700-705. http://www.ncbi.nlm.nih.gov/pmc/articles/
PMC3117991/?tool=pubmed
Aitcheson, N. et al. 2005. VSG switching in Trypanosoma brucei: antigenic variation analysed using RNAi in the
absence of immune selection. Molecular Microbiology 57(6): 1608–1622. http://www.ncbi.nlm.nih.gov/pmc/
articles/PMC1618954/
Moore, D. et al. 2002 African trypanosomiasis in travelers returning to the United Kingdom. Emerging Infectious
Disease 8(1): 74-76. http://wwwnc.cdc.gov/eid/article/8/1/01-0130.htm
Reinitz, D.M., and J.M. Mansfield. 1990. T-cell-independent and T-cell-dependent B-cell responses to exposed variant
surface glycoprotein epitopes in Trypanosome-infected mice. Infection and Immunity 58(7): 2337-2342. http://
www.ncbi.nlm.nih.gov/pmc/articles/PMC258817/pdf/iai00055-0323.pdf

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Image of African mask in title block © Mcsxp74 | Dreamstime.com , ID# 19806652. Case copyright held by the National
Center for Case Study Teaching in Science, University at Buffalo, State University of New York. Originally published June 21,
2012. Please see our usage guidelines, which outline our policy concerning permissible reproduction of this work.

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