El documento trata sobre la miocarditis infecciosa, en particular la causada por el parásito Trypanosoma cruzi, que provoca la enfermedad de Chagas. Describe el ciclo de vida del parásito T. cruzi y cómo invade y daña los cardiomiocitos, causando miocarditis aguda y potencialmente una cardiopatía dilatada crónica. También explica los síntomas clínicos de la enfermedad de Chagas aguda y crónica, así como las opciones de tratamiento y prevención disponibles.
12. Enfermedades infecciosas y parasitarias
Age-standardised disability-adjusted life year (DALY) rates from Infectious and parasitic diseases by country (per 100,000 inhabitants).
Death and DALY estimates for 2004 by cause for WHO Member States (Persons, all ages) (2009-11-12)
13. Pérdida de años de vida ajustados en función de la discapacidad
10 principales causas mundiales
24. Lane 1: Molecular weight markers lambda
HindIII.
Lane 2: Negative control, mummy Eg-1 muscle
tissue.
Lane 3: Positive control, mummy For-1 heart
tissue.
Lane 4: Mummy Az-75, T-43, esophagus tissue.
Lane 5: Mummy Az-75, T-133, C-1, heart tissue.
Lane 6: T. cruzi stock tulahuen from culture.
Lane 7: Trypanosome-free human blood.
Lane 8: Control reaction, H2O.
Am J Phys Anthropol 108:401–407, 1999
Co-evolución
30. Epimastigotas
Teixeira DE, Benchimol M, Crepaldi PH, de Souza W (2012) Interactive Multimedia to Teach the Life Cycle of Trypanosoma cruzi, the Causative
Agent of Chagas Disease. PLoS Negl Trop Dis 6(8): e1749. doi:10.1371/journal.pntd.0001749
http://www.plosntd.org/article/info:doi/10.1371/journal.pntd.0001749
31. Teixeira DE, Benchimol M, Crepaldi PH, de Souza W (2012) Interactive Multimedia to Teach the Life Cycle of Trypanosoma cruzi, the Causative
Agent of Chagas Disease. PLoS Negl Trop Dis 6(8): e1749. doi:10.1371/journal.pntd.0001749
http://www.plosntd.org/article/info:doi/10.1371/journal.pntd.0001749
Amastigotas
32. Teixeira DE, Benchimol M, Crepaldi PH, de Souza W (2012) Interactive Multimedia to Teach the Life Cycle of Trypanosoma cruzi, the Causative
Agent of Chagas Disease. PLoS Negl Trop Dis 6(8): e1749. doi:10.1371/journal.pntd.0001749
http://www.plosntd.org/article/info:doi/10.1371/journal.pntd.0001749
Tripomastigotas
65. Infección por T. cruzi
Regulación de la respuesta inmune
Homeostasis
inmunológica,
Persistencia
del parásito,
Fibrosis
Control del
parásito, daño
colateral
IFN-g, TNF-a,
NO, ROS, IL-
17, MMP,
TLR, NLR
IL-10, TGF-b,
NO, T-reg
72. Cobertura de las acciones de
control de la transmisión 1996-2000
73. Lecturas sugeridas
• Maria C. Bewley et al. Structural Analysis of the Mechanism of
Adenovirus Binding to Its Human Cellular Receptor, CAR.
Science 19 November 1999,
• Anis Rassi Jr, Anis Rassi, José Antonio Marin-Neto. Chagas
Disease. Lancet2010; 375: 1388–40
• Caryn Bern et al. Evaluation and Treatment of Chagas Disease
in the United States. A Systematic Review. JAMA.
2007;298(18):2171-218
• Ribeiro, A. L. et al. Diagnosis and management of Chagas
disease and cardiomyopathy. Nat. Rev. Cardiol. 9, 576–589
(2012)
• Dirceu E. Teixeira et al. Interactive Multimedia to Teach the
Life Cycle of Trypanosoma cruzi, the Causative Agent of
Chagas Disease. PLoS Negl Trop Dis. 2012 Aug;6(8):e174
Notas del editor
FIGURE: 4-C H/T SIZE CASE Email Line H/T Combo Revised REG F Enon 2nd 3rd 1 of 2 ARTIST: ts 22p3 The number of years lost to disability and premature death (disability- adjusted life-years) for the 13 major neglected tropical diseases were calculated according to a method we described previously. 4 The disability-adjusted life-years for the other conditions are based on data from the World Health Organization. 23 The ranking of disease burdens is based on data in Hotez. 5
Figure 1. Yardstick for Financial Resource Allocation Based on the Global Burden Awarded to Each Disease in TDR’s Portfolio in the2001–2002 Biennium(Top) and the 2007–2008 Biennium(Bottom). The figures show that the diseases fall into two relatively distinct groups,(i) well-funded (i.e., malaria and tuberculosis), and (ii) less well-funded, including leprosy, which is now targeted for elimination as a threat in publichealth. Note the particularly low amounts currently allocated to schistosomiasis and lymphatic filariasis in relation to the estimated global burden ofthese diseases. doi:10.1371/journal.pntd.0000244.g001
Isolation of Trypanosoma cruzi DNA in 4,000-Year-OldMummified Human Tissue From Northern Chile
Fig. 2. Apoptoticcells drive parasite growthwithinmacrophages. Trypomastigoteforms of Tryp-anosoma cruzi infectmacrophages, escape vacuoles and multiply in thecytoplasm. (a) Macrophageactivation: type 1 cytokinesactivatemacrophages and induce L-arginineconversionto NO, byiNOS.NO killsthe parasite and controlsmacrophageinfection. (b) Macrophagedeactivation: T cells die byapoptosis in thecourse of theimmune response toinfection. Apoptoticcellsengage avb3 and inducemacrophagesto produce PGE2 and TGF-b. TGF-b shifts L-argininemetabolismtowardsornithineand putrescineproduction. Putrescinebursts parasite growthwithinmacrophages. TGF-b also blocksNO productionbyactivatedmacrophages and, therefore, allows parasite survival, growth and spread.Abbreviations: avb3 integrin, thevitronectin receptor; IFN-g, interferon g; iNOS, inducible nitricoxide synthase; Mf, macrophage; NO, nitric oxide; ODC, ornithinedecarboxylase; PGE2,prostaglandin E2; Th1, T helper 1; TGF-b, transforminggrowth factor b; TNF-a, tumor necrosisfactor a.
Figure 3 Stages and causes of death in Chagas heartdisease. AV, atrioventricular; LAH, left anterior hemiblock; PVCs, premature ventricularcontractions; RBBB, rightbundlebranch block; VA, ventricular arrhythmias; WMA, wallmotionabnormality.