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16-18 million infected 100 million at risk 50,000 deaths annually leading cause of cardiac disease in S. and Central America Trypanosoma cruzi causative.

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Presentation on theme: "16-18 million infected 100 million at risk 50,000 deaths annually leading cause of cardiac disease in S. and Central America Trypanosoma cruzi causative."— Presentation transcript:

1 16-18 million infected 100 million at risk 50,000 deaths annually leading cause of cardiac disease in S. and Central America Trypanosoma cruzi causative agent of Chagas disease discovered by Carlos Chagas named organism after mentor, Oswaldo Cruz determined life cycle described salient features of disease

2 Genera Triatoma Rhodnius Panstrongylus Common Names triatomine bugs reduviid bugs assassin bugs kissing bugs conenose bugs

3 Triatomine Vectors >100 species can transmit 3 primary vectors T. dimidiata (central Am.) R. prolixis (Colombia and Venezuela) T. infestans (southern cone countries)

4 metacyclic trypomastigotes excreted in triatomine feces entry via bite wound, mucous membranes (eg., eyes), hair follicles

5 metacyclic trypomastigotes excreted in triatomine feces entry via bite wound, mucous membranes (eg., eyes), hair follicles blood-stream trypomastigotes are non-dividing trypomastigotes invade host cells and convert to amastigotes

6 amastigotes replicate by binary fission

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8 amastigotes transform to trypomastigotes release of trypomastigotes and reinvasion of host cells ingestion of blood-stream trypomastigotes by triatomine

9 conversion to epimastigotes and replication in midgut migration to hindgut and transformation to trypomastigote

10 Modes of Transmission

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12 early defecation (i.e., during triatomine feeding) colonization of human habitats ­adobe walls ­thatched roofs para-domiciliary cycles ­animal stalls adjacent to domicile proximity to sylvatic cycle Factors Influencing Human Transmission

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17 triatomine bugs found in U.S. parasite common in wild animals 5 confirmed autochthonous cases why no autochthonous transmission? late defecaters zoophillic vectors better houses Trypanosoma cruzi in the U.S. inefficient transmission + limited vector-human contact

18 improvement of human dwellings separation of animal stalls from house health education insecticides synthetic pyrethroids eg., Southern Cone Initiative major in Chagas (T. infestans) little affect with R. prolixis gentian violet in blood for transfusions Chagas Control

19 Clinical Course of Chagas Acute Phase ­active infection ­1-4 months duration ­most are asymptomatic (children most likely to be symptomatic) Indeterminate Phase ­10-30 years of latency ­relatively asymptomatic with no detectable parasitemia ­seropositive Chronic Phase ­10-30% of infected exhibit cardio- myopathy or megasyndromes

20 Acute Phase Features 1-2 week incubation period local inflammation Romañas sign chagoma symptoms can include: fever, malaise, lymphadenopathy, hepatosplenomegaly, nausea, diarrhea acute, often fatal, myocarditis develops in a few individuals high parasitemias in myofibrils

21 long latency characterized by seropositivity and no parasitemia higher prevalence of ECG abnormalities in asymptomatic seropositive persons progressive development of abnormalities right bundle branch block left anterior hemiblock clinical presentations include: arrhythmias and conduction defects congestive heart failure thromboembolic phenomenon Chronic Chagas' Cardiomyopathy

22 cardiomegaly hypertrophy* apical aneurysm (left ventricle) extensive fibrosis* cellular infiltration *correlates best with cardiac symptoms Pathology

23 cardiomegaly hypertrophy* apical aneurysm (left ventricle) extensive fibrosis* cellular infiltration *correlates best with cardiac symptoms Pathology

24 prevalence varies by geographical zones Chili, central Brazil colon and esophagus most frequently affected megaesophagus painful swallowing regurgitation megacolon severe constipation Megaviscerae

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26 destruction of parasympathetic neurons dilation non-Chagas Chagas C = heart S = colon E = esophagus

27 Basis of Pathogenesis altered immune response? (Th1 Th2 switch correlated with severe disease) chagasic factor or toxin? (proposed by not found)

28 history of living in infested house bug bite, chagoma, Romaña's sign cardiac or gastro- intestinal symptoms imaging detection of parasite (acute stage) serology (chronic stage) DIAGNOSIS

29 parasite detection direct examination stained blood smears inoculation into mice in vitro culture xenodiagnosis PCR serological tests hemagglutination immunofluorescence ELISA complement fixation DIAGNOSIS

30 acute stage –nifurtimox (8-16 mg/kg/day, 60-90 days) –benzidazole (5-7 mg/kg/day, 30-120 days) –allopurinol (experimental) –azole antifungal agents (experimental) chronic stage –treat symptoms TREATMENT

31 Viotta et al (1994) Am. Heart J. 127:151 benznidazole treatment (5 mg/kg/day, 30 d) followed for 8 years

32 Lauria-Pires et al (2000) AJTMH 63:111 Brasília street cleaners treatment standard treatment with nifurtimox or benznidazole 10 year follow up treated vs. untreated: no parasitiological cure (PCR) no sero-negative conversion no ECG improvements administration of nitroderivatives severe side effects compliance problems

33 Trypanosoma rangeli can be confused with T. cruzi non-pathogenic for humans pathogenic for triatomines mode of transmission? found in both salivary glands and feces


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