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Trypanosoma cruzi causative agent of Chagas disease

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Presentation on theme: "Trypanosoma cruzi causative agent of Chagas disease"— Presentation transcript:

1 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 16-18 million infected 100 million at risk 50,000 deaths annually leading cause of cardiac disease in S. and Central America

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

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


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

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

10 Modes of Transmission


12 Factors Influencing Human Transmission
‘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





17 Trypanosoma cruzi in the U.S.
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 inefficient transmission + limited vector-human contact

18 Chagas Control 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

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
Romaña’s 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 Chronic Chagas' Cardiomyopathy
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

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

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

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


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 DIAGNOSIS 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)

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

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

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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