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Human African Trypanosomiasis : Sleeping Sickness in Sub-Saharan Africa Matthew Malone 3/9/2012

Human African Trypanosomiasis : Sleeping Sickness in Sub-Saharan Africa Matthew Malone 3/9/2012. Learning Goals. Understand the causes, risk factors, and modes of transmission for Human African Trypanosomiasis (HAT)

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Human African Trypanosomiasis : Sleeping Sickness in Sub-Saharan Africa Matthew Malone 3/9/2012

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  1. Human African Trypanosomiasis: Sleeping Sickness in Sub-Saharan Africa Matthew Malone 3/9/2012

  2. Learning Goals • Understand the causes, risk factors, and modes of transmission for Human African Trypanosomiasis (HAT) • Know the role of armed conflict in the rise of infection rates throughout Africa • Use past HAT outbreak patterns and causes to understand the implications for future infection

  3. The Problem • Multiple HAT outbreaks have occurred over the last century. • Armed conflict in Africa has escalated disease rates in recent years. • Continued displacement of populations may cause many more outbreaks. • Displacement widens the geographic disease spread.

  4. Causal Agents • Caused by the protozoan TrypanosomaBrucei • Has three subspecies: • Trypanosomabruceigambiense • Trypanosomabruceirhodesiense • Trypanosomabruceibrucei(animals only)

  5. Vector Biology • The vector for HAT is the tsetse fly • Biological Vector • Inhabits rural areas • Bites during daytime hours • Both males and females are capable of carrying and transmitting the disease.

  6. Vector Biology Cont’d • Tsetse flies belong to the genus Glossina • Glossinacontains 3 subgroups • Glossina(includes G. morsitansgroup) • Nemorhina(includes G. palpalis group) • Austenina(includes G. fuscagroup)

  7. Vector Biology Cont’d • Vectors of T.b. gambiense • G. palpalis & G. tachinoidesgroups • Vectors of T.b. rhodesiense • G. morsitans, G. swynnertoni, & G. pallidipesgroups

  8. Reservoirs T.b. gambiense T.b. rhodesiense

  9. Transmission Cycle

  10. Risk Factors • Civil Disturbance/War • Cattle Movements • Population Movements/Migrations (Refugees) • Reduced Health Program Financing • Rural Living Environment

  11. Case Study: Uganda HAT Outbreak • Began in the late 1980s and persisted through 2005 • Refugees migrated from Uganda to Zaire and Sudanacquired infection • Refugees migrated back to Uganda accompanied by infected Sudanese refugeesspread infection

  12. Case Study Cont’d

  13. Epidemiology • In 1986, it was estimated that approx. 70 million people lived in areas conducive to disease transmission • HAT affects 36 countries in sub-Saharan Africa • According to the World Health Organization, HAT causes ~40,000 deaths in Africa annually

  14. Epidemiology Cont’d • The total amount of reported HAT cases has decreased substantially over time. • 1998: ~40,000 reported cases; >250,000 actual cases • 2004: ~18,000 reported cases; between 50,000 and 70,000 actual cases • 2010: ~7,000 reported cases; ~30,000 actual cases • Cases involving T.b. rhodesienseare much rarer than those involving T.b. gambiense.

  15. Epidemiology Cont’d

  16. Geographical Distribution • 1998- World Health Organization states that there are over 200 active foci of HAT between latitude 15 degrees north and 15 degrees south (“tsetse belt”). • T.b. gambienseis mostly found in western and central Africa. • Over 95% of the cases of human infection found in the Democratic Republic of Congo, Angola, Sudan, Central African Republic, Chad, and northern Uganda. • T.b. rhodesienseis found mostly in eastern and southernAfrica. • Over 95% of the cases of human infection occur in Tanzania, Uganda, Malawi, and Zambia.

  17. Geographical Distribution Cont’d

  18. Geographical Distribution/Conflict • The resurgence of HAT in several countries has been attributed to conflict and/or war. • Cases of HAT have been seen to occur significantly more often in countries where there is conflict, internationalized civil war, and/or high political terror.

  19. Geographical Distribution/Conflict Cont’d

  20. Geographical Distribution/Conflict Cont’d • Forced population movement increases transmission. • Migration causes trypanosomes to circulate from high-incidence to low-incidence areas. • Conflict causes breakdown of control measures and surveillance, increasing disease spread

  21. References 1. Pepin J., Meda H. The epidemiology and control of human African trypanosomiasis. AdvParasitol, 49 (2001), pp. 71–132 2. Human African trypanosomiasis (sleeping sickness). Available at http://www.who.int/mediacentre/factsheets/fs259/en/. Accessed March 8, 2012. 3. Smith D., Pepin J., Stich A. Human African trypanosomiasis: an emerging public health crisis. Br Med Bull, 54 (1998), pp. 341–355 4. BrunR., Blum J., Chappuis F., Burri C. Human African trypanosomiasis. Lancet (2009), pp. 148–159 5. SimarroP., Jannin J., Cattand P. Eliminating human African trypanosomiasis: where do we stand and what comes next? PLoS Med. 5, e55 (2008), pp. 174–180

  22. References Cont’d 6. Parasites- African Trypanosomiasis (also known as Sleeping Sickness). Available at http://www.cdc.gov/parasites/sleepingsickness/. Accessed March 8, 2012. 7. Berrang-Ford L, Martin O, Maiso F, Waltner-Toews D, McDermott J (2006) Sleeping sickness in Uganda: revisiting current and historical distributions. Afr Health Sci 6: 223–231 8. KuzoeFAS. (1993) Current situation of African trypanosomiasis. Acta Trop. 54: 153-162 9. MacGregorP., Matthews K. New discoveries in the transmission biology of sleeping sickness parasites: applying the basics. J. Mol. Med., 88 (2010), pp. 865–871

  23. References Cont’d 10. Berrang-Ford L., Breau L. Conflict and human trypanosomiasis. Soc. Sci. Med. (2010), pp. 398–407

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