apply knowledge of cellular and molecular processes to understand infectious disease mechanisms

Addresses Course Outcomes #1, #2, #3

  • recognize the use of the scientific method to weigh evidence, make decisions, and solve problems
  • apply knowledge of cellular and molecular processes to understand infectious disease mechanisms
  • synthesize knowledge of microbial pathogenesis and disease prevention methods and communicate this knowledge to the community

A scientific case study is a short summary of an event or personal experience that ends in a “mystery”—in this case, one that you will solve using your own research and the clues provided within the case study. For this project, you will evaluate a patient-centered case study that explores a mysterious bacterial or viral illness. The case study will include a set of questions to guide your analysis.

Your paper should include the following:
 

Paper format:
Once you have gathered all of your information, you will organize your case study analysis into an essay of 1,000 to 1,500 words (not including original case study OR references). The essay should include in-text citations and references formatted in APA style.

Format Guidelines: (please separate “pages” with a horizontal line in the text box)
 – Page 1: Should include the following:
 – Name
 – Case study text you were given (do not include the questions)

Page 2: Begin your paper here

Brief introduction to the disease and the bacterial or viral cause of the disease.

Use the evidence provided in the case study and the information you have gathered from references to support your conclusions.

The answers to the case study questions should be worked into your final document in a logical, well-organized manner. Think of the questions as a guide to help you with the content of your paper. You should NOT simply answer these questions one by one in your paper.

Paper should be 1,000 to 1,500 words (not including original case study or references).

Use in-text citations and include reference citations at the end of the paper

References:
 You must have a minimum of two outside sources to support your evaluation.
 These can consist of any of the following: books, textbooks, scholarly journal articles, and websites run by reputable government organizations (such as the CDC or NIH).
 You may have additional references as well. All of your references should be no more than six years old (published in 2005 or later).

Citations: 

You should include BOTH in-text citations and a final reference page formatted in APA style. Please see http://www.umuc.edu/library/citationguides.shtml for additional information on how to format citations and references in APA style.
 All work must be original work written by you and your group members. Your paper may be checked for plagiarism, so please make a concerted effort to use and cite your sources appropriately. Any submitted work that is not your own, or incidences of plagiarism, will be reported to UMUC administration.

ebola_general.pdf

Page 1“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

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Part I –What Is a Virus? “I can’t believe I’m a college sophomore,” thought Terry in amazement while taking the train back home for the summer. “Th e school year went by so fast, but I made it through even though I had to change my major.”

A text popped up on Terry’s smartphone, “Terry, when r u going on ur trip? Let’s meet up before u go.” Terry recognized that the message was from Alex, a long-time friend from high school. “Leaving in a week,” Terry quickly texted back. “Never been on a trip outside of the US and can’t wait to work with doctors and nurses to help sick people. Alex, let’s meet up Fri.”

After a week of seeing family and friends, Terry was off to the west coast of Africa for ten weeks. Th is would be a life- changing experience. Th e agency placed Terry in a rural site where residents had limited access to medical care. Th e locals sometimes traveled miles to be seen at their clinic. Th e health care professionals on the team were unbelievably positive and devoted to educating and providing patients with the best care possible. Residents came in with many types of ailments. Terry’s responsibilities included greeting patients and their families, bandaging wounds, and providing additional assistance to doctors and nurses as needed.

Just like the school year, the summer experience seemed as though it was over in no time. Terry was about to return home when unexpected news came. Terry’s team was contacted by the Centers for Disease Control and Prevention (CDC) and notifi ed that they had likely been exposed to a patient infected with the Ebola virus as there was an outbreak near the medical relief site. Th e patient who had contracted the virus had died. Struck with fear, Terry quickly tried to determine which patient it could have been and her likelihood of being infected, but she found this nearly impossible to fi gure out. As a precaution, all individuals on the team returning to the US had to be screened and undergo a 21-day quarantine where they would be monitored for any Ebola-like symptoms. Not doing so could potentially place others at risk for contracting this deadly virus.

“I need to fi nd out more about viruses so that I can understand what’s going on,” thought Terry as she reached for her general biology textbook. Glancing through the section on virology, she was surprised to discover that viruses are tiny particles considered to be non-living since they cannot metabolize energy, do not create waste, do not grow, and require host cells to multiply. Indeed, in order to replicate, viruses hijack the machinery present within the cells that they infect. Th e additional viral particles produced inside host cells can exit and infect other cells. “Th ese viruses seem kind of creepy,” thought Terry. “Th ey’re like parasites to cells.”

Terry continued reading:

General EditionGeneral Edition

by Tracie M. Addy, Yale School of Medicine Teaching and Learning Center, Yale University Linda M. Iadarola , Department of Biological Sciences, Quinnipiac University Derek Dube, Department of Biology, University of Saint Joseph

The Ebola WarsThe Ebola Wars In every battle there comes a time when both sides consider themselves

beaten, then he who continues the attack

wins. –Ulysses S. Grant–

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Page 2“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

Viruses have either a DNA or RNA genome, which can be single- or double-stranded. Th ese genomes are housed in a capsid made of proteins. Viruses can be classifi ed by their specifi c genomes and the unique features of their capsids, including shape and protein constituents. Some viruses have lipid envelopes derived from host membranes that enclose the virus particle, while others do not. Surface glycoproteins on these membranes, or spike proteins protruding from the viral capsid in non-enveloped viruses, can play a role in viral attachment and entry into the host cell.

Terry spent the next few minutes summarizing the information she had just read.

Questions

1. Which structural features are in common to all viruses, and which are not? Complete the table below to answer this question based upon the information provided in the case.

Shared Attributes Diff erences

2. Why are viruses considered parasites?

3. Examine the diagram of the viral particle below. Label all of the important structures on this virus that you identifi ed in the table above.

4. Design an imaginary viral particle. Create a diagram of your virus and label its major features. Your virus should have a diff erent capsid shape (e.g., icosahedral, helical, complex) than the one above and be non-enveloped.

Figure 1. A general viral particle.

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Page 3“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

Part II – How Could a Virus Have Entered? Terry considered what she had learned so far. “So the Ebola virus could be inside my cells? But how? How exactly could a virus get inside? It seems to start at the plasma membrane… I’d better keep reading.”

In the fi rst step of infection, viral proteins interact specifi cally with host cells. Diff erent viruses like infl uenza, rabies and even Ebola each have unique glycoproteins on their surface that bind only to specifi c receptors on the particular host cells they infect. For example, the infl uenza virus uses the HA (hemagglutinin) protein for binding to the host cell receptors on respiratory epithelial cells. A rabies virus relies on the G protein protruding out of its viral envelope to attach to the host cell receptors of neurons. Ebola virus uses GP to bind to the host cell receptors on a wide variety of cells, beginning with the macrophages and dendritic cells of the lymphatic system. Once viruses attach to the host cell in this very specifi c manner, there are three major ways for them to complete the second stage of infection, entry into the host cell. Th e fi rst is by direct injection of its genome (DNA or RNA) into the host cell at the cell surface. Th e second is the binding of the virus to the plasma membrane, followed by the fusion of the viral envelope with the host membrane to transfer the viral genome (DNA or RNA) into the host cell. Th e third way is for the virus to bind to the host cell membrane and become internalized into the host cell via the endocytic pathway.

“Th is is very strange,” she thought.

Questions

1. Why is viral attachment to the host cell specifi c between one virus and one type of cell?

2. List several types of host cells and the associated virus that binds to the host cell.

3. What are three major ways in which a virus enters a host cell to deliver its genome?

4. Formulate a hypothesis as to why there is more than one mechanism of viral entry into host cells.

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Page 4“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

Part III – The Battle between Viruses and Cells “Now if the virus and its genetic material have gotten inside of my cells, what happens next?” Determined to fi nd out, Terry read further and paraphrased the text.

“Th e next step is viral synthesis. So, it looks like once the virus enters my cells it hijacks the cell machinery including many of my cells’ enzymes and ribosomes normally used to make my own proteins. Th e virus does not have these proteins and structures so it relies heavily on the host cell to do the work for it. Th is process involves not only replication of the genome, but also transcription of viral genes and translation of viral proteins. I remember learning about transcription and translation in biology class. Now this is starting to come together. Still, this really bothers me to think that the Ebola virus could be in my cells doing all this crazy stuff .

“So after viral synthesis comes viral assembly. Th is step sounds a lot like a factory, because the viral proteins and genomes are put together to make complete viral particles. But then they still have to get out of the cells … .

“Ah, I see, this step is called viral release and can diff er between viruses. Some viruses with envelopes bud from the host cell, taking pieces of the host cell membrane with viral proteins incorporated within, while others leave by exocytosis in vesicles that bud from the endoplasmic reticulum or Golgi. Viruses without envelopes lyse (break open) the host cell and leave that way, often killing the cell in the process.”

“It’s almost like a battle between the virus and my cells. Th ese viruses invade the cell to take over, and the cell doesn’t even know it right away! Th en a whole army of new viruses leave the cell and go out to invade and do battle with all my other nearby cells.”

Questions

1. Describe the essential cell “machinery” that viruses use to make a new virus.

2. Why do viruses need the machinery to make more viruses? Why can’t they replicate on their own?

3. What are the structures that need to be put together during viral assembly? Consider the key structural components of viruses described earlier.

4. How does the army of new viruses get out of the cell to infect the nearby cells?

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Page 5“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

5. Examine the diagram below depicting viral infection of a typical cell.

a. Identify all (fi ve) of the steps used by viruses to get into the cell, make copies of viral proteins and leave the cell as an army of viruses out to attack nearby cells.

i. __________________________

ii. __________________________

iii. __________________________

iv. __________________________

v. __________________________

b. Label the two cellular components indicated on the diagram.

Figure 2. Viral infection of a typical cell.

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Page 6“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

Part IV – The Ebola Wars In the middle of searching for more information on the Ebola virus, Terry began to feel gravely ill. Feverish, achy, nauseated and weak, Terry’s worst fears came true—the symptoms were consistent with an Ebola virus infection. While she now knew that Ebola virus could not be transmitted through the air, she recalled that during her trip to West Africa she had a small cut on her hand while she was bandaging a patient who had high fever and was hemorrhaging. Th e exchanged fl uid may have contained Ebola virus particles that infected Terry’s cells. After fi ve days of illness including repeated vomiting and extreme pain, Terry wondered if this was the end. A decision was made to transport Terry to a special facility for treatment and isolation.

Ebola is an enveloped, single-stranded RNA virus with a capsid and matrix made of VP40 and other viral proteins. Ebola packages its own RNA-dependent RNA polymerase (L) (see Figure 3). Like many viruses, Ebola goes through

the processes of viral attachment, entry, synthesis, assembly and release. Recall that the Ebola virus has the protein GP on its surface, which is required for attachment and entry to the host cell.

Once the virus attaches to the host cell, a series of events through the endocytic pathway leads to its entry into the cell. Th is means the virus comes into the cell enclosed in a vesicle from the plasma membrane and gets delivered to endosomes. Inside the endosome, the virus relies on the low pH to modify GP and help it fuse with the membrane of the endosome. Once the viral genome is inside the cell cytoplasm, viral synthesis can begin, including genome replication, transcription of viral genes, and translation of viral proteins. Th e packaged Ebola L enzyme is important for initiating these synthesis steps. One protein produced that is important to the structure of the Ebola virus is called VP40, which determines the fi lamentous viral shape and interacts with the viral capsid. VP40 is made at the ribosomes of Terry’s infected host cells, along with other Ebola virus proteins like the RNA-dependent RNA polymerase (L) and the envelope glycoprotein (GP). Later, the VP40 proteins assemble with the other viral factors, like the viral genome,

Figure 3. Ebola virus.

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Page 7“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

at the cell’s plasma membrane and acquire GP proteins that are already inserted in the host cell membrane. At this point, the complete viruses can bud from the cell to spread the infection.

Th is very battle was occurring between Terry’s cells and the Ebola virus.

Questions

1. Examine the diagram (Figure 4, next page) showing the life cycle of the Ebola virus. a. Label the fi ve major steps used by Ebola virus to infect cells. In what specifi c ways are these similar or

diff erent from those you labeled in the general virus life cycle?

i. __________________________

ii. __________________________

iii. __________________________

iv. __________________________

v. __________________________

Key similarities and diff erences:

b. Label the key viral and cellular factors in the indicated areas of the diagram. Describe each of their roles.

2. Formulate a hypothesis as to what would happen to viral replication and budding from the cell if the ribosomes did not make VP40.

3. What is one structural component of the Ebola virus to target for a vaccine that prevents infections like Terry’s? Explain your answer. Keep in mind the Ebola virus structures and that vaccines are developed to prevent viral infections (for example, the fl u vaccine contains a weakened form of the infl uenza virus that does not cause disease).

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Page 8“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

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Page 9“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

Part V – Treatment Terry’s doctor knew quick action was necessary to help her survive the Ebola infection. Th e doctor had four options to treat Terry’s condition: a vaccine, a standard antiviral medication, an immunotherapy-based method of treatment, and serum from an Ebola patient who had fully recovered.

Th e fi rst option, a vaccine in clinical trials, could potentially provide protection against a viral infection when used prior to contracting the disease. Vaccines typically introduce the body to an antigen, consisting of the dead virus, or parts of a virus, such as a specifi c glycoprotein from the viral protein coat/envelope. Th ese non-self antigens are considered foreign to the body and invoke an immune response where antibodies are made against the viral protein in the vaccine. Once antibodies are made and circulated throughout the body, they can attach to the viral antigens and the immune system destroys the antigen. Th is immune response takes time.

When considering the second option, Terry’s doctor thought about antiviral therapies for other viruses, like the fl u. She knew that with infl uenza infection, the antiviral medicine Tamifl u™ was only eff ective if administered within the fi rst 48 hrs of infection. Unfortunately, Terry was in late stages of the disease, and there were no such approved Ebola- specifi c antiviral medicines currently available for use.

Th e third option was immunotherapy with the investigational treatment ZMapp.™ ZMapp is a treatment method that uses three unique antibodies against Ebola GP made in tobacco plants. While there had not been any large-scale human trials at the time of Terry’s infection, when these antibodies were injected into Ebola-infected mice and rhesus macaque primates, the animals showed increased survival. As such, ZMapp was thought to be a potentially eff ective antiviral/immunotherapy-based treatment for Ebola infections in humans, and in a few cases was used to treat human Ebola patients during the 2014 outbreak. Although the mechanism of action for ZMapp had not been elucidated yet, researchers believed that since the antibodies in ZMapp bound to the glycoprotein (antigen) on the Ebola virus, it prevented viral attachment to the cells and thus did not allow entry or viral replication.

A fi nal option would be to give Terry serum from a patient who had recovered from an Ebola infection of the same strain. Th is serum would be rich with Ebola-specifi c antibodies to enhance Terry’s immune response. However, this method of treatment required identifying an Ebola virus survivor who had blood type compatibility with Terry and who was willing and able to donate serum in a timely fashion.

Question

1. Synthesize the information provided above. Come up with an argument as to the best treatment plan for Terry.

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Page 10“Th e Ebola Wars: General Edition” by Addy, Iadarola, & Dube

Case copyright held by the National Center for Case Study Teaching in Science, University at Buff alo, State University of New York. Originally published February 9, 2016. Please see our usage guidelines, which outline our policy concerning permissible reproduction of this work. Licensed image in title block ©Ezume Images | Fotolia, id#93050805.

Part VI – Recovery Terry’s symptoms cleared and she was virus free. Th e battle was now over and Terry’s cells won. One would never know whether it was the treatment, Terry’s own immune system, or a combination of the two that won the war against Ebola. In the end, Terry survived the potentially-deadly infection and was able to return home without any long-term eff ects, other than a newfound understanding and appreciation of how viruses, like Ebola, replicate and cause disease.

Victory at all costs, victory in spite of all terror, victory however long and hard the road may be;

for without victory, there is no survival.

—Winston Churchill—

•http://sciencecases.lib.buffalo.edu/cs/http://sciencecases.lib.buffalo.edu/cs/collection/uses/

safari.pdf

Page 1“African Illness” by Kevin M. Bonney

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

African Illness: A Case of Parasites?

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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Page 2“African Illness” by Kevin M. Bonney

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 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 sickness. All of the patient’s symptoms are explained 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?

Figure 1. T. brucei trypomastigotes (blood stage form) in a blood smear.

Image courtesy of Centers for Disease Control and Prevention/ Dr. Mae Melvin, ID# 10167 in CDC Public Health Image Library (PHIL). Public domain.

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Page 3“African Illness” by Kevin M. Bonney

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 blood every day,” explained the doctor, “we would likely notice that the parasitemia level would steadily increase for a period of time, perhaps one week, then the parasitemia level would fall drastically over one or 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 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.”

Time

N um

be r o

f p ar

as ite

s pe

r m l o

f b lo

od

Figure 2. Parasitemia level vs. time

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Page 4“African Illness” by Kevin M. Bonney

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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2

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.

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.pdfhttp://sciencecases.lib.buffalo.eduhttp://sciencecases.lib.buffalo.eduhttp://sciencecases.lib.buffalo.edu/cs/collection/uses/

 

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