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Trypanosoma cruzi, Screenshot_2024_0324_133353, Screenshot_2024_0324…
Trypanosoma cruzi
Pathogenicity
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1° lesion -
acute regional lymphadenitis ,fever
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Chronic - Arrhythmias , palpitations , chest pain,
Oedema , dizziness , syncope & dyspnoea
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Lab diagnosis
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NNN medium , Yager's medium
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AB detection
- ELISA , IFA , IHA , Western blot ,CFT ,
Radio immunoprecipitation assay , PCR , CLIA
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Discovery
April 15, 1909 - "Carlos Chagas" (1878-1934), young researcher at (IOC; Oswaldo Cruz Institute), announced to the scientific world the discovery in Lassance, state of Minas Gerais, of a new tropical disease caused by the protozoan "Trypanosoma cruzi "(also described by him in 1908)
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Host
- Vertebrate host - Human
- Invertebrate host - " Reduviid bugs/
Kissing bugs / Triatomine bugs
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Lifecycle
- During a blood meal, an infected Triatominae insect vector (or kissing bug) releases trypomastigotes in its feces near the site of the bite wound.
- Trypomastigotes enter the host through the wound or through intact mucosal membranes (eg, conjunctiva). Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes.
- The amastigotes multiply by binary fission.
- They differentiate into trypomastigotes, then burst out of the cell and enter the bloodstream. Bloodstream trypomastigotes can infect cells in various tissues; there, they transform into intracellular amastigotes and cause symptomatic infection. In the bloodstream, trypomastigotes, unlike African trypanosomes, do not multiply. Multiplication resumes only when the parasites enter another cell or are ingested by another vector.
- The kissing bug becomes infected by feeding on human or animal blood that contains circulating parasites.
- The ingested trypomastigotes transform into epimastigotes in the vector's midgut.
- The parasites multiply in the midgut.
- In the hindgut, they differentiate into infective metacyclic trypomastigotes, which are excreted in feces.
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