An Analysis of Trypanosomiasis Infection within Sub-Saharan Africa and How its Impact can be Suppressed Rockefeller F. Cooper II, PhD. Student Walden University Ph 8165-2 Instructor: Dr. Stephen Arnold FALL, 2009 An Analysis of Trypanosomiasis Infection within Sub-Saharan Africa and How its Impact can be Suppressed By Rockefeller F. Cooper II FALL, 2009

The Government of Liberia: Stakeholders The Government of Liberia: Ministry of Health: Public Health Officials Healthcare Givers Monrovia City Hall Corp As a Liberian, I have decided to do a presentation on the eradication of trypanosomiasis from the west African Republic of Liberia. Apart from being patriotic, Liberia our home country is a fairly small as it comprises 111,370 km² of which 96,320 km² is land and 15,050 km² is water. Geographically, this can be considered as a small landmark and can be use as a perfect model for eradication of the disease. I strongly believe that public health officials and healthcare givers that are under the Ministry of Health and officials of the Monrovia City Hall Corporation in collaboration with our government will benefit from this presentation.

Learning Objectives What is trypanosomiasis? What causes it and how is it transmitted? Who is at risk? What are the symptoms? How do we prevent it? How do we control it? How do we treat it? Understanding the etiology and geography. Before we get to the lay out of presentation, I will like to ensure that the following objectives are considered for learning purposes as stated below: Insuring that there is a high level of understanding of the disease. Identifying common health errors that enables one to be victimized by the disease. Identifying those are subjected to being infected by the disease Identifying the signs and symptoms that are affiliated with trypanosomiasis, so as to enable make early detection of an infection. Finding an ideal method to prevent trypanosomiasis infection. Finding a means to suppress the widespread of trypanosomiasis. Treating the disease with the best drugs available along with their specific dosage. To enable the viewers understand the etiology and geographical distribution of the disease.

African Trypanosomiasis Etiology of African Trypanosomiasis Outline I Introduction African Trypanosomiasis Etiology of African Trypanosomiasis Geographical Distribution Mode of Transmission Symptoms Human African Trypanosomiasis African Animal Trypanosomiasis Outline I As we discuss about trypanosomiasis today, listed below is the format of how my presentation will follow. After an introduction to the subject matter, we will cover the etiology of the disease, followed by its geographical distribution. Next we will focus on the mode of transmission and then have a look at the symptoms of trypanosomiasis relating to both humans and animals.

Outline II Prevention A-B-C Method Control use of insecticide traps and screens Treatment References Outline II As we continue with this presentation we will look at the “ABC METHOD” of prevention as well as the use of insecticide, traps and screen to control the widespread of trypanosomiasis. Finally, a host of possible treatments will be discussed followed by a review of our sources so that we can have an idea as to where our information were obtained. The purpose of this presentation is to serve as a means of educating people on the effects of Trypanosomiasis and how the disease can be prevented from it’s widespread. It is also with great hopes that my presentation will serve as an “eye-opener” for those who are suffering from the disease or who have family members that are victims of the disease as well. This presentation is geared towards helping mainly my fellow sub-Saharan Africans since the disease has it’s most devastating effect with in that region. As a Liberian from West Africa, I have decided to use my government as a stakeholder through its Ministry of Health and the Environmental Protection Agency.

Approximately, 66 million people are victims (Dias,1999). Introduction I Trypanosomiasis is commonly known as “sleeping sickness”(Dias, 1999). In cattle and other domestic animals, the disease is referred to as Nagana (Dias,1999). Approximately, 66 million people are victims (Dias,1999). Reference: Dias, J.C.P (1999). The evolution of Chagas disease (American Trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121. Introduction Trypanosomiasis, which is commonly known as “sleeping sickness”, is a disease that can be both endemic and epidemic at times. This chronic disease is caused by a blood parasite of the genus Trypanosoma that happens to be a protozoon. The main vector for this parasite is a grayish-brown insect about the size of a honeybee called the tsetse-fly which consumes and spreads infected blood based parasites called trypanosomes after feeding off a host and victim respectively, which includes humans and animals. In cattle and other domestic animals, the disease is referred to as Nagana - a Zulu term for being in a depress state(Dias,1999). Looking at the variation of this disease with respect to where they are found, in Central and West Africa serves as host to the Trypanosoma brucei gambiense, which is the most common causal agent of the disease. In East and Southern Africa, there is the Trypanosoma brucei Rhodesiense. Approximately, 66 million people (men, women and children) within the Sub-Saharan region are victims of the Human African Trypanosomiasis, which runs within 36 countries(Dias,1999). Reference: Dias, J.C.P (1999). The evolution of Chagas disease (American Trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121.

Introduction II Acute and chronic phase. Origin was unknown as caravanners noticed prevailing symptoms of the disease (Dias,1999). The disease infiltrated the western, eastern and southern parts of Africa Colonial masters organized campaigns to prevent and control trypanosomiasis. This effort turned out to be successful due to the use pentamidine, and agronol prevention (Dias,1999). Reference: Dias, J.C.P (1999). The evolution of Chagas disease (American Trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121. This disease, which has an acute and chronic ill- causing phase, has plagued the Dark Continent since the 14th century during the days of the West African Kingdom of Mali. Though its origin was unknown, caravanners noticed prevailing symptoms of the disease in frequent visitors of other southern African kingdoms. It was during this same period that the mortal effect of this disease was noticed due to epidemic that caused the lost of about 500,000 lives (Dias,1999). The disease had then infiltrated the western, eastern and southern parts of Africa and as a means of combating the infectious rate, colonial masters organized campaigns that were geared to prevent and control the widespread of Trypanosomiasis. This effort turned out to be successful due to the use of the drug pentamidine, which was given as a shot to terminate the parasite. Also was the use of agronol prevention, which consisted of clearing bushes and flushing stagnant waters so as to destroy the breeding grounds for the tsetse-fly (Dias,1999). Reference: Dias, J.C.P (1999). The evolution of Chagas disease (American Trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121.

Introduction III Trypanosomiasis was suppressed but reemerged after African countries started to obtain their independence. as they could not maintained the financial burden of suppressing the disease (Dias,1999). Trypanosomiasis causes economical instability due to death infliction on cattle as a result of anemia, loss of condition and emaciation. Disease is caused by: Trypanosoma congolense, Trypanosoma vivax and Trypanosoma brucei brucei. (Grove, 1990). References: Dias, J.C.P (1999). The evolution of Chagas disease (American Trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121. Grove, A.T. (1990). The Changing Geography of Africa. Oxford, England: Oxford University Press. Unfortunately, as the incidence of Trypanosomiasis was suppressed, it reemerged after African countries started to obtain their independence. This was due to the fact that they could not maintained the financial burden of suppressing the disease (Dias,1999). Trypanosomiasis on the other hand, causes economical instability as well. This occurs by death infliction on cattle due to anemia, loss of condition and emaciation. This form of the disease is caused by the following protozoal parasites: Trypanosoma congolense, Trypanosoma vivax and Trypanosoma brucei brucei. Infections can occur concurrently with multiple species (Grove, 1990). As trypanosomiasis affects humans and animals within the confinement of the continent, they are distinguished based upon the location of the attack, i.e.; the region of occurrence. For people living in the western and central parts of Africa, once bitten by tsetse flies, which serve as vectors for the disease causing parasites, they become infected with the “sleeping sickness disease”. The parasite of this infection is the T. gambiense. On the other hand, East and Southern Africans are infected through the same means but through another trypanosome called T. Rhodesiense (Legros,2002). Though incidences of African trypanosomiasis are approximated to be within the range of 300,000- 500,000 cases per year, the World Health Organization (W.H.O.) notes only 25,000- 45,000 of the total. This mishap is a result of the poor health protocols that exist in a lot of these countries since poverty prevents them from having the required infrastructures in place (Legros,2002). Reference: Dias, J.C.P (1992). Epidemiology of Chagas disease. Retrieved October 5, 2006, from Foreign Animal Diseases Web site: http://www.dbbm.fiocruz.br/tropical/chagas/chapter4.html Dias, J.C.P (1999). The evolution of Chagas disease (American trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121. Grove, A.T. (1990). The Changing Geography of Africa. Oxford, England: Oxford University Press.

Etiology of African Trypanosomiasis Since Trypanosomiasis in animals are caused by a number of different trypanosomes, or more precisely, protozoan that can lead to animal mortality, the origin of this disease can be viewed independently as the genus (Trypanosoma) of the family (Trypanosomatidae) has several species (Grove,1990). As discussed earlier, this disease is caused by a blood parasite of the genus Trypanosoma. The main vector for this parasite is a grayish-brown insect about the size of a honeybee called the tsetse-fly which consumes and spreads infected blood based parasites called trypanosomes after feeding off a host and victim respectively, which includes humans and animals. When feeding on a host, the tsetse fly injects parasites into tissues beneath the skin. These parasites then enters the bloodstream via the lymphatic system where they transform into metacyclic trypomastigotes (2008). At this point, through the means of binary fission, they spread to other parts of the body, thus infecting the bloodstream. During another blood meal by an uninfected vector, which in this case would be the fly, the infected blood enters the midgut of the fly, transform into procyclic trypomastigotes at which point in time binary multiplication occurs as well. There is later transformation to epimastigotes which then gets into the salivary glands of the fly where multiplication continues as well. All of this occurs in about 21 days (2008). Reference: Grove, A.T. (1990). The Changing Geography of Africa. Oxford, England: Oxford University Press. Dias, J.C.P (1999). The evolution of Chagas disease (American Trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121. (2008,Dec 5). African Trypanosomiasis. Retrieved October 7, 2009, from CDC Web site: http://www.dpd.cdc.gov/dpdx/html/TrypanosomiasisAfrican.htm (2008,Dec 5). African Trypanosomiasis. Retrieved October 7, 2009, from CDC Web site: http://www.dpd.cdc.gov/dpdx/html/TrypanosomiasisAfrican.htm

Geographical Distribution African Trypanosomiasis: Tsetse flies are between latitude 15 0 North and 20 0 South. Central and West Africa serves as host to the Trypanosoma brucei gambiense, which is the most common causal agent of the disease. In East and Southern Africa, there is the Trypanosoma brucei Rhodesiense. Reference: Legros, D (2002).Treatment for human African Trypanosomiasis-present situation and needs for research and development. The Lancelet Infectious Diseases. 2, 437-440. Dias, J.C.P (1999). The evolution of Chagas disease (American Trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121. Geographical Distribution: African Trypanosomiasis resides in the tropical terrains of the continent. This is because the endemic zones of the tsetse flies are between latitude 15 0 North and 20 0 South from the southern edge (Algeria, Libya and Egypt) of the Sahara desert to the northern parts of southern Africa (Zimbabwe, Angola and Mozambique). Despite this boundary setting, T.vivax has eloped beyond the African tsetse fly belt by means of mechanical vector transmission to Central and South America as well as other parts of the Caribbean (Legros,2002). Central and West Africa serves as host to the Trypanosoma brucei gambiense, which is the most common causal agent of the disease whereas Trypanosoma brucei Rhodesiense. applies to East and Southern Africa. Reference: Legros, D (2002).Treatment for human African Trypanosomiasis-present situation and needs for research and development. The Lancelet Infectious Diseases. 2, 437-440. Dias, J.C.P (1999). The evolution of Chagas disease (American Trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121.

Mode of Transmission References: Human African Trypanosomiasis: Glossina are the vectors African Animal Trypanosomiasis: The vectors are Glossina palpalis, Glossina fusca and Glossina morsitans Other vectors are of the genus Tabanus, Haematopota, Chrysops, Liperosia and Stomoxys References: Carlier, Yves (2004). Chagas Disease. Retrieved October 10, 2009, from the chagaspace group Web site: http://chagaspace.org/eng/chagas/index.htm Legros, D (2002).Treatment for human African Trypanosomiasis-present situation and needs for research and development. The Lancelet Infectious Diseases. 2, 437-440. Human African Trypanosomiasis (HAT): Tsetse flies of the genus Glossina serves as the vector for parasites relating to this disease. These flies acquire a blood meal from an organism- human or animal (Dias,1999). If the organism being preyed upon is currently serving as a host to the trypanosomes, the fly automatically becomes infested with the disease-causing parasite during the meal period. This is because as the vector acquires the parasite in its salivary glands whiles feeding on blood from the host(Carlier,2004). Secondly, during a subsequent meal, the target victim becomes infected due to the transmission of trypanosomes into the host and the process is repetitious for future victims(Carlier,2004). Adjacently, there are fomite (inanimate objects that can transmit diseases) vectors such as surgical instruments, needles and syringes that can aid in transmission when unsterilized(Legros,2002). African Animal Trypanosomiasis (AAT): Just as in human transmission, the parasites do replicate in tsetse flies as well. In this aspect, the species primarily involved are Glossina palpalis, Glossina fusca and Glossina morsitans (Carlier,2004). When a fly bites an infected animal, trypanosomes are transmitted into the salivary glands of the fly permanently. Upon feeding on another animal, be it infected or not, the fly injects some of the parasites into the animal through the salivary glands. Other flies of the genus Tabanus, Haematopota, Chrysops, Liperosia and Stomoxys also serve as transmitters for the parasites and are termed mechanical vectors (Carlier,2004). References: Carlier, Yves (2004). Chagas Disease. Retrieved October 10, 2009, from the chagaspace group Web site: http://chagaspace.org/eng/chagas/index.htm Legros, D (2002).Treatment for human African Trypanosomiasis-present situation and needs for research and development. The Lancelet Infectious Diseases. 2, 437-440.

symptoms Human African Trypanosomiasis: Chancre develops from bite. Other manifestations are: fever rash severe headache severe fatigue painful muscles and joints Edema around eyes and hand Winterbottom’s sign weight loss Reference: Moore, A (2004). Human African Trypanosomiasis: a reemerging public health threat. Washington, D.C: ASM Press. African Animal Trypanosomiasis: Infertility Abortion Anemia Weight loss Intermittent fever Reference: Grove, A.T. (1990). The Changing Geography of Africa. Oxford, England: Oxford University Press. Human African Trypanosomiasis: Revelations of an infection(s) can be seen anywhere from a few weeks to months and even up to years after a painful bite has been administered by the tsetse fly. This bite develops into a red sore called chancre (Moore,2004). Some signs of the disease are insomnia at night, long sleep during the day, fever, rash, severe headache, severe fatigue, painful muscles and joints and edema around the eyes and hands(Stich,2002). As the infection progresses, victims might experience swollen lymph nodes on the back of their necks (Winterbottom’s sign), weight loss, slurred speech progressive confusion, fluctuation in ability to concentrate, seizure and a change of personality(Trail,1985). Further progression that involves the invasion of the Central Nervous System professes difficulty in walking and talking. If no treatment is rendered, death will definitely serve as a final result(Stitch,2002). African Animal Trypanosomiasis: The symptoms in animals are severe due to the chronic infections that are inflicted upon them by the trypanosomes. Some major symptoms include infertility and abortion, anemia, edema, weight loss and intermittent fever(Grove,1990). As the disease progresses, poor nutrition, significant immunosuppression; concurrent infections complicating the disease occurs as well. Stress can also follow suite(Grove,1990). References: Grove, A.T. (1990). The Changing Geography of Africa. Oxford, England: Oxford University Press. Moore, A (2004). Human African Trypanosomiasis: a reemerging public health threat. Washington, D.C: ASM Press. Stich, A (2002).Human African Trypanosomiasis. BMJ. 325, 203-06. Trail, J.C.M (1985). Productivity of Boran cattle maintained by chemoprophylaxis under Trypanosomiasis risk. Retrieved April 10, 2009, from Economic trade-offs between milk and meat production Web site: http://www.fao.org/wairdocs/ILRI/x5527E/x5527e00.HTM

Prevention A-B-C Method: Awareness of Risk Bite Avoidance Chemoprophylaxis References: Carlier, Yves (2004). Chagas Disease. Retrieved October 10, 2009, from the chagaspace group Web site: http://chagaspace.org/eng/chagas/index.htm Legros, D (2002).Treatment for human African Trypanosomiasis-present situation and needs for research and development. The Lancelet Infectious Diseases. 2, 437-440. A-B-C method: I. Awareness of Risk: People should inquire about the level of tsetse fly infestation within an environment before visiting. This is a hint mainly for travelers (Legros,2002). II. Bite Avoidance: Bites should be avoided so as to prevent infections and implementing the following strategies as follows can do this: A. Wearing protective clothing such as long-sleeved shirts and pants that are made of thick material. An example would be a pair of jeans and khaki shirt. This is appropriate since the tsetse fly can bite through thin clothing (Legros,2002). B. Use of bed nets when sleeping, regardless if its day or night. C. Avoid riding in open vehicles (trucks, pickup, and jeeps) so as to avoid being a feeding source. This aspect is mainly for movement through the hinterlands. D. Avoid bushy areas as much as possible since they serve as potential breeding grounds for the flies that tend to bite when bothered. III. Chemoprophylaxis: Since prevention is better than cure, the use of prophylaxes would be a suitable recommendation as there are no vaccines yet available. An example of such drug that is used mainly by cattle owners is samorin. Other involved are cymelarsan, a very arsenic but highly effective in treating T.b. brucei and pyrithidium bromide, used against T.vivax and T.congolense. These drugs can last from three to six months(Carlier,2004). References: Carlier, Yves (2004). Chagas Disease. Retrieved October 10, 2009, from the chagaspace group Web site: http://chagaspace.org/eng/chagas/index.htm Legros, D (2002).Treatment for human African Trypanosomiasis-present situation and needs for research and development. The Lancelet Infectious Diseases. 2, 437-440.

Other Control & Methods Insecticide Traps and Screen References: (2004, Oct 19). Trypanosomiasis. Retrieved April 10, 2009, from Public Health Agency of Canada Web site: http://www-micro.msb.le.ac.uk/224/Trypano.html Moore, A (2004). Human African Trypanosomiasis: a reemerging public health threat. Washington, D.C: ASM Press. In order to diminish the current population of tsetse flies thus placing a halt on their growth and development, the approaches below can be considered. Use of insecticide: A. Residual Insecticide: This approach has to do with a one time spraying of residences using DDT and dieldrin(2004). B. Non- residual Insecticide: As the term implies, this form of insecticide usage has to do with outdoor spraying of fields with the use of aircrafts. For this process, the chemical uses are endosulphan and a newer and much more toxic insecticide, pyrethroids (2004). Traps and Screens: These tools are use to capture the vector as the flies are moving about aimlessly This methodology is highly successful when these instruments are bright colored since they serve as attractants. It has also been noticed that bovine’s breath serve as an attractant also due to its component of carbon dioxide and acetone (Moore,2004). References: (2004, Oct 19). Trypanosomiasis. Retrieved April 10, 2009, from Public Health Agency of Canada Web site: http://www-micro.msb.le.ac.uk/224/Trypano.html Moore, A (2004). Human African Trypanosomiasis: a reemerging public health threat. Washington, D.C: ASM Press.

Treatment Drugs Species Dosage Route Common side effects Phase acute Pentamidine isethionate T. gambiense acute 7-10 doses of 4mg/kg per day IM Diarrhea Dizziness Headache Upset stomach Nausea Suramin sodium T. rhodisiense 5mg/kg on the 1st day, 10 on the 3rd and 20 on the 5th,11th, 23rd and 30th IV Renal failure Anaphylactic shocks Signs of neurotoxicity Severe cutaneous reactions Melasoprol chronic 3-4 series of 3-4 injections per day Reactive encephalopathic syndrome Elfornithine 400mg/kg per day in 4 daily infusions for 1-2 wks. Pancytopenia Convulsion Hallucination Nifurtimox T. cruzi Oral Anorexia Neurological problems Treatment Trypanosomiasis being an old disease has been treated for decades. This disease has two phases (acute and chronic) and is treated precisely with regards to the stage of infection and the trypanosome that is involved. The table below gives a layout of drugs use to treat the disease6. A unique difference can be seen in their use and side effects as well (2006). In addition to this, each drug is dose, specie and route specific. Reference: (2006, Feb 8). West African Trypanosomiasis. Retrieved April 8, 2009, from Division of parasitic Diseases Web site: http://www.cdc.gov/NCIDOD/dpd/parasites/trypanosomiasis/factsht_ea_trypanosomiasis.htm

What have we learned ? The nickname for trypanosomiasis is “sleeping sickness”. It is an infectious disease that can be transmitted by the tsetse fly. Two phases are involved. Infection is specie specific with regards to the geography. Transmission of the disease into humans and animals are not of the same species as symptoms vastly differs as well. Prevention using the “ABC Method” as well as traps, screen and insecticide. Different types of drugs. What have we learned ? After our study on trypanosomiasis, we will all agree that we now know a nickname for the disease as well as the vector that can spread the infection as well. We learned also that there is an acute and chronic phase during an infection by the vectors which are specific depending on the part of Africa where the infection occurs like the T. gambiense and T. rhodisiense. In addition to these facts, we discovered that different flies are responsible for transmission into both humans and animals. When it comes to prevention, we also talked about awareness, bite avoidance, the use of chemoprophylaxis in addition to screen, traps and insecticide. If prevention fails, we saw a list of drugs such as Melasoprol, Suramin sodium, Pentamidine isethionate, etc

References "American Trypanosomiasis of Chagas Disease." Public Health Agency of Canada. 13 June 2001. Public Health Agency of Canada. Retrieved October 10, 2009, from http://www.phac-aspc.gc.ca/tmp-pmv/info/am_trypan_e.html. Carlier, Yves (2004). Chagas Disease. Retrieved October 10, 2009, from the chagaspace group Web site: http://chagaspace.org/eng/chagas/index.htm Dias, J.C.P (1999). The evolution of Chagas disease (American trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121. Dias, J.C.P (1992). Epidemiology of Chagas disease. Retrieved October 5, 2006, from Foreign Animal Diseases Web site: http://www.dbbm.fiocruz.br/tropical/chagas/chapter4.html Grove, A.T. (1990). The Changing Geography of Africa. Oxford, England: Oxford University Press. Legros, D (2002).Treatment for human African trypanosomiasis-present situation and needs for research and development. The Lancelet Infectious Diseases. 2, 437-440. References 1."American Trypanosomiasis of Chagas Disease." Public Health Agency of Canada. 13 June 2001. Public Health Agency of Canada. Retrieved October 10, 2009, from http://www.phac-aspc.gc.ca/tmp-pmv/info/am_trypan_e.html . 2. Carlier, Yves (2004). Chagas Disease. Retrieved October 10, 2009, from the chagaspace group Web site: http://chagaspace.org/eng/chagas/index.htm 3. Dias, J.C.P (1999). The evolution of Chagas disease (American trypanosomiasis) control after 90 years since Carlos Chagas discovery. Memorias do Instituto Oswaldo Cruz. 1, 103-121. 4. Dias, J.C.P (1992). Epidemiology of Chagas disease. Retrieved October 5, 2006, from Foreign Animal Diseases Web site: http://www.dbbm.fiocruz.br/tropical/chagas/chapter4.html 5. Grove, A.T. (1990). The Changing Geography of Africa. Oxford, England: Oxford University Press. 6. Legros, D (2002).Treatment for human African trypanosomiasis-present situation and needs for research and development. The Lancelet Infectious Diseases. 2, 437-440.

References II Mare, C.J. (1998). Foreign animal diseases. Retrieved October 10, 2009, from The Gray Book Web site: http://www.vet.uga.edu/VPP/gray_book/FAD/index.htm Mare, C.J. (1998). In foreign animal diseases. Richmond, VA: United States Animal Health Association. Moore, A (2004). Human African Trypanosomiasis: a reemerging public health threat. Washington, D.C: ASM Press. Stich, A (2002).Human African Trypanosomiasis. BMJ. 325, 203-06. Trail, J.C.M (1985). Productivity of Boran cattle maintained by chemoprophylaxis under Trypanosomiasis risk. Retrieved October 10, 2009, from Economic trade-offs between milk and meat production Web site: http://www.fao.org/wairdocs/ILRI/x5527E/x5527e00.HTM (2004, Oct 19). Trypanosomiasis. Retrieved October 10, 2009, from Public Health Agency of Canada Web site: http://www-micro.msb.le.ac.uk/224/Trypano.html (2006, Feb 8). West African Trypanosomiasis. Retrieved October 8, 2009, from Division of parasitic Diseases Web site: http://www.cdc.gov/NCIDOD/dpd/parasites/trypanosomiasis/factsht_ea_trypanosomiasis.htm 7. Mare, C.J. (1998). Foreign animal diseases. Retrieved October 10, 2009, from The Gray Book Web site: http://www.vet.uga.edu/VPP/gray_book/FAD/index.htm 8. Mare, C.J. (1998). In foreign animal diseases. Richmond, VA: United States Animal Health Association. 9. Moore, A (2004). Human African Trypanosomiasis: a reemerging public health threat. Washington, D.C: ASM Press. 10. Stich, A (2002).Human African Trypanosomiasis. BMJ. 325, 203-06. 11. Trail, J.C.M (1985). Productivity of Boran cattle maintained by chemoprophylaxis under Trypanosomiasis risk. Retrieved October 10, 2009, from Economic trade-offs between milk and meat production Web site: http://www.fao.org/wairdocs/ILRI/x5527E/x5527e00.HTM 12. (2004, Oct 19). Trypanosomiasis. Retrieved October10, 2009, from Public Health Agency of Canada Web site: http://www-micro.msb.le.ac.uk/224/Trypano.html . 13. (2006, Feb 8). West African Trypanosomiasis. Retrieved October 8, 2009, from Division of parasitic Diseases Web site: http://www.cdc.gov/NCIDOD/dpd/parasites/trypanosomiasis/factsht_ea_trypanosomiasis.htm

Bibliography for further reading Cooper, Rockefeller (2007). Prevention and Control of Selective Tropical Diseases. Baltimore, MD: Publish America (2008,June 8). West African Trypanosomiasis. Retrieved October 10, 2009, from CDC Web site: http://www.cdc.gov/ncidod/dpd/parasites/trypanosomiasis/factsht_wa_trypanosomiasis.htm (2009). Trypanosomiasis, Africa. Retrieved October 7, 2009, from World Health Organization Web site: http://www.who.int/topics/trypanosomiasis_african/en/ Kioy, D., & Jannin , N (2004). Human African Trypanosomiasis. Nature Reviews Microbiology. 2, 186-187. Bibliography Cooper, Rockefeller (2007). Prevention and Control of Selective Tropical Diseases. Baltimore, MD: Publish America (2008,June 8). West African Trypanosomiasis. Retrieved October 10, 2009, from CDC Web site: http://www.cdc.gov/ncidod/dpd/parasites/trypanosomiasis/factsht_wa_trypanosomiasis.htm (2009). Trypanosomiasis, Africa. Retrieved October 7, 2009, from World Health Organization Web site: http://www.who.int/topics/trypanosomiasis_african/en/ Kioy, D., & Jannin , N (2004). Human African Trypanosomiasis. Nature Reviews Microbiology. 2, 186-187.