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Trypanosomes cruzi, • Patient may be screened for elevated levels of IgM…
Trypanosomes cruzi
Morphology
Epimastigote / Promastigote- These protozoa are motile and fusiform and have a blunt posterior end and a pointed anterior end from which a single flagellum projects
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The kinetoplast complex of the epimastigote form, in contrast, is located centrally, just in front of the vesicular nucleus.
The flagellum runs anteriorly in the free edge of an undulating membrane before passing out of the cell
In the mammalian host, hemoflagellates appear as trypomastigotes (Trypanosoma) or amastigotes (Leishmania, T cruzi).
The former circulates in the bloodstream and closely resemble the epimastigote form, except that the kinetoplast complex is in the posterior end of the parasite
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Lab dignosis
• Microscopic examination of lymph node aspirates, blood, or cerebrospinal fluid for the presence of trypomastigotes.
• Early in the disease, actively motile organisms can often be seen in a simple wet mount preparation smear.
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• A card agglutination test for trypanosomiasis (CATT), which can be performed on fingerstick blood, can provide serologic confirmation within minutes.
• Subspecies-specific DNA probes may prove useful for the identification of organisms in clinical specimens
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Lifecycle
During a blood meal on the mammalian host, an infected tsetse
metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and fly (genus Glossina) injects pass into the bloodstream
Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission ..
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The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host , .
In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes . multiplication by binary fission .
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Rarely, T. b. gambiense may be acquired congenitally if the mother is infected during pregnancy.
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Pathogenisis
Lymphadenitis- Multiplication of the trypomastigotes at the inoculation site produces a localized inflammatory lesion. After the development of this chancre, organisms spread through lymphatic channels to the bloodstream, inducing a proliferative enlargement of the lymph nodes.
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Prevention
Most effective agent is a highly toxic arsenical, melarsoprol (Mel B).
Ornithine decarboxylase inhibitor, eflornithine (DFMO) appears capable, when used
alone, or in combination with suramin, of curing CNS disease
If CNS is not involved, less toxic agents, such as suramin, pentamidine, or
eflornithine, can be used.
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• Patient may be screened for elevated levels of IgM in the blood and spinal fluid or specific trypanosomal antibodies by a variety of techniques.
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