Vl 3 Trypanosoma cruzi Flashcards
How does Trypanosoma cruzi invade its host cells?
1) has as many ligands as it could possibly have on surface
examples:
- muzines (defense against digestive enzymes)
- fibronectine receptors ⇒ help adherering to the host cell (macrophages or muscle)
2) induces “induced phagocytosis” through PIP3 to get in or directly by recruiting lysosomes (unknown how it survives or get’s out of the macrophage)
Which organ is affected most in a Trypanosoma cruzi infection?
the heart
- muscle cells are immune privileged
- first cardiac arrhythmia, and heart enlargement, then thinning of heart walls and inflammation in 40% of the infections (heart can erupt)
Describe the two pathomechanisms that can contribute to the chronic, pathogenic complications elicited by a Trypanosoma cruzi infection.
1) parasite let’s host cells erupt after proliferation⇒ can disturb peristalsis by destroying ganglia of smooth muscles
2. 1) TLR2 immune response ⇒ sialic acid transfered from host cells to parasite surface, but recognized in chronic phase with TLR2 ⇒ recruiting of NK-cells which induces inflammation ⇒ can lead to autoimmune reaction (because an epitope of parasites protein resembles an extracellular receptor in heart muscles)
How can Chagas disease be controlled?
quick chemotherapeuthic intervention after infection with: Lampit, Benznidazol
Prophylaxis:
mosquito nets
improvement of housing (keine Strohdächer ⇒ Ziegeldächer)
check of blood donors
additional barriers between hosts and humans (hängematte)
Describe the life cycle of Trypanosoma cruzi
1) triatome bug bites human and leave feces next to bite
2) scratching get’s trypomastigotes into blood stream
3) macrophage and muscle cell invasion
4) amastigote transformation (asexual replicate life stage)
5) trypomastigote transformation free in blood again
6) triatome bug takes up parasite
7) conversion to epimastigote followed by trypomastigote conversion in bug gut
