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group_2_presentation_1_-_chagas_disease [2018/02/03 00:37]
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group_2_presentation_1_-_chagas_disease [2018/02/03 00:45] (current)
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 Abnormal ECG: Abnormal Q waves; AV blocks; low QRS voltage; SSS (Sick SInus Syndrome)-malfunctioning sinus node; PVCs (extra heartbeats)(Rassi,​ 2014)> ​ Abnormal ECG: Abnormal Q waves; AV blocks; low QRS voltage; SSS (Sick SInus Syndrome)-malfunctioning sinus node; PVCs (extra heartbeats)(Rassi,​ 2014)> ​
  
-<box 43% round |>​{{:​chagas6.png?​520|}}</​box|Figure 7. Image of Tachycardia ECG>+<box 43% round |>​{{:​chagas6.png?​520|}}</​box|Figure 7. Image of Tachycardia ECG (Rassi, 2014)>
  
-<box 43% round |>​{{:​chagas7.png?​520|}}</​box|Figure 8. Image of Bradyarrhythmia ECG>+<box 43% round |>​{{:​chagas7.png?​520|}}</​box|Figure 8. Image of Bradyarrhythmia ECG (Rassi, 2014)>
  
-<​box ​50% round |>​{{:​chagas8.png?​600|}}</​box|Figure 9. Segmental/​Global Dilated Cardiomyopathy>​+<​box ​43% round |>​{{:​chagas8.png?​520|}}</​box|Figure 9. Segmental/​Global Dilated Cardiomyopathy ​(Rassi, 2014)>
  
-<​box ​50% round |>​{{:​chagas9.png?​600|}}</​box|Figure 10. Associated megaesophagus and megacolon>​+<​box ​43% round |>​{{:​chagas9.png?​520|}}</​box|Figure 10. Associated megaesophagus and megacolon ​(Rassi, 2014)>
  
 **In Summary:** **In Summary:**
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 An infected vector is one that has trypomastigotes in their hindgut. Upon taking a blood meal from humans, they leave their feces on the skin and this is how trypomastigotes enter from kissing bugs to humans. Once they are in the human body, they lose their flagella and transform in the ideal. This is the ideal life cycle for them to reproduce exponentially within the cells. Once they have fully infected the cell, they transform back into trypomastigotes and burst out of the cell and enter the bloodstream. Once in the bloodstream,​ they can access other organs and once again transform into amastigotes inside the cell to replicate and infect the organ. Keep in mind that if a non-infected T.cruzi takes a blood meal from an infected human, they will become infected as well (Center of Disease Control and Prevention, 2015). An infected vector is one that has trypomastigotes in their hindgut. Upon taking a blood meal from humans, they leave their feces on the skin and this is how trypomastigotes enter from kissing bugs to humans. Once they are in the human body, they lose their flagella and transform in the ideal. This is the ideal life cycle for them to reproduce exponentially within the cells. Once they have fully infected the cell, they transform back into trypomastigotes and burst out of the cell and enter the bloodstream. Once in the bloodstream,​ they can access other organs and once again transform into amastigotes inside the cell to replicate and infect the organ. Keep in mind that if a non-infected T.cruzi takes a blood meal from an infected human, they will become infected as well (Center of Disease Control and Prevention, 2015).
  
-<​box ​65% round |>{{ :​chagas_18.png|}}</​box|Figure 12. Image of the vector'​s life cycle (Center of Disease Control and Prevention, 2015)>+<​box ​50% round |>{{ :​chagas_18.png?600|}}</​box|Figure 12. Image of the vector'​s life cycle (Center of Disease Control and Prevention, 2015)>
 ======Mechanism====== ======Mechanism======
  
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 ======References====== ======References======
 +Bern, C. (2015). Chagas’ disease. New England Journal of Medicine, 373(5), 456-466.
  
-  - Bern, C. (2015). Chagas’ disease. New England Journal of Medicine, 373(5), 456-466. +Bonney, K. M., & Engman, D. M. (2008). Chagas heart disease pathogenesis:​ one mechanism or many?. Current molecular medicine, 8(6), 510-518.* 
-  - Bonney, K. M., & Engman, D. M. (2008). Chagas heart disease pathogenesis:​ one mechanism or many?. Current molecular medicine, 8(6), 510-518.* + 
-  ​- ​Calvet, C. M., Melo, T. G., Garzoni, L. R., Oliveira Jr, F. O., Neto, D. T. S., NSL, M., ... & Pereira, M. C. (2012). Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction. Frontiers in immunology, 3. +Calvet, C. M., Melo, T. G., Garzoni, L. R., Oliveira Jr, F. O., Neto, D. T. S., NSL, M., ... & Pereira, M. C. (2012). Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction. Frontiers in immunology, 3. 
-  ​- ​Center of Disease Control and Prevention (2015). Chagas. Retrieved from https://​www.cdc.gov/​parasites/​chagas/​biology.html  + 
-  ​- ​Chaves, A. T., Estanislau, J. D. A. S. G., Fiuza, J. A., Carvalho, A. T., Ferreira, K. S., Fares, R. C. G., ... & da Costa Rocha, M. O. (2016). Immunoregulatory mechanisms in Chagas disease: modulation of apoptosis in T-cell mediated immune responses. BMC infectious diseases, 16(1), 191. +Center of Disease Control and Prevention (2015). Chagas. Retrieved from https://​www.cdc.gov/​parasites/​chagas/​biology.html  
-  ​- ​Gaspar, L., B Moraes, C., H Freitas-Junior,​ L., Ferrari, S., Costantino, L., Paola Costi, M., ... & Cordeiro-da-Silva,​ A. (2015). Current and future chemotherapy for Chagas disease. Current medicinal chemistry, 22(37), 4293-4312. Retrieved from https://​research-repository.standrews.ac.uk/​bitstream/​handle/​10023/​9920/​Gaspar_2016_Current_CurrMedChem_4293.pdf?​sequence=1  + 
-  ​- ​Loury, E. (2012). Chagas'​ disease can cast a silent, lifelong shadow. Los Angeles Times. Retrieved from http://​articles.latimes.com/​2012/​jul/​08/​local/​la-me-chagas-20120708 +Chaves, A. T., Estanislau, J. D. A. S. G., Fiuza, J. A., Carvalho, A. T., Ferreira, K. S., Fares, R. C. G., ... & da Costa Rocha, M. O. (2016). Immunoregulatory mechanisms in Chagas disease: modulation of apoptosis in T-cell mediated immune responses. BMC infectious diseases, 16(1), 191. 
-  ​- ​Moncayo, Á. (2010). Carlos Chagas: biographical sketch. Acta tropica, 115(1), 1-4. + 
-  ​- ​Montgomery, S. (2017). Heart Failure at Age 46? Centers for Disease Control and Prevention. Retrieved from https://​blogs.cdc.gov/​global/​2017/​04/​14/​heart-failure-at-age-46/​ +Gaspar, L., B Moraes, C., H Freitas-Junior,​ L., Ferrari, S., Costantino, L., Paola Costi, M., ... & Cordeiro-da-Silva,​ A. (2015). Current and future chemotherapy for Chagas disease. Current medicinal chemistry, 22(37), 4293-4312. Retrieved from https://​research-repository.standrews.ac.uk/​bitstream/​handle/​10023/​9920/​Gaspar_2016_Current_CurrMedChem_4293.pdf?​sequence=1  
-  ​- ​Rassi, A., (2014) Chagas’ Heart Disease. World Congress of Cardiology Scientific Sessions. + 
-  ​- ​Rassi, A., & Marin-Neto, J. A. (2010). Chagas disease. The Lancet, 375(9723), 1388-1402. +Loury, E. (2012). Chagas'​ disease can cast a silent, lifelong shadow. Los Angeles Times. Retrieved from http://​articles.latimes.com/​2012/​jul/​08/​local/​la-me-chagas-20120708 
-  ​- ​Rassi Jr, A., Rassi, A., & Marin-Neto, J. A. (2009). Chagas heart disease: pathophysiologic mechanisms, prognostic factors and risk stratification. Memorias do Instituto Oswaldo Cruz, 104, 152-158. + 
-  ​- ​Steverding, D. (2014). The history of Chagas disease. Parasites & vectors, 7(1), 317. +Moncayo, Á. (2010). Carlos Chagas: biographical sketch. Acta tropica, 115(1), 1-4. 
-  ​- ​Teixeira, D. E., Benchimol, M., Crepaldi, P. H., & de Souza, W. (2012). Interactive multimedia to teach the life cycle of Trypanosoma cruzi, the causative agent of Chagas disease. PLoS neglected tropical diseases, 6(8). + 
-  ​- ​Teixeira, A.R.L., Nitz, N., Guimaro, M.C., Gomes, C., & Santos-Buch,​ C.A. (2006). Chagas disease. Postgrad Med J, 82 (974): 788-798. +Montgomery, S. (2017). Heart Failure at Age 46? Centers for Disease Control and Prevention. Retrieved from https://​blogs.cdc.gov/​global/​2017/​04/​14/​heart-failure-at-age-46/​ 
-  ​- ​World Health Organization (2017). Chagas Disease. Retrieved from: http://​www.who.int/​mediacentre/​factsheets/​fs340/​en  ​+ 
 +Rassi, A., (2014) Chagas’ Heart Disease. World Congress of Cardiology Scientific Sessions. 
 + 
 +Rassi, A., & Marin-Neto, J. A. (2010). Chagas disease. The Lancet, 375(9723), 1388-1402. 
 + 
 +Rassi Jr, A., Rassi, A., & Marin-Neto, J. A. (2009). Chagas heart disease: pathophysiologic mechanisms, prognostic factors and risk stratification. Memorias do Instituto Oswaldo Cruz, 104, 152-158. 
 + 
 +Steverding, D. (2014). The history of Chagas disease. Parasites & vectors, 7(1), 317. 
 + 
 +Teixeira, D. E., Benchimol, M., Crepaldi, P. H., & de Souza, W. (2012). Interactive multimedia to teach the life cycle of Trypanosoma cruzi, the causative agent of Chagas disease. PLoS neglected tropical diseases, 6(8). 
 + 
 +Teixeira, A.R.L., Nitz, N., Guimaro, M.C., Gomes, C., & Santos-Buch,​ C.A. (2006). Chagas disease. Postgrad Med J, 82 (974): 788-798. 
 + 
 +World Health Organization (2017). Chagas Disease. Retrieved from: http://​www.who.int/​mediacentre/​factsheets/​fs340/​en  ​
  
  
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