Flashcards in Chagas Disease Deck (24):
What parasite causes Chagas disease?
Outline the life cycle of the parasite
Trypomastigotes transform into epimastigotes in the hind gut of a triatomine bug. They replicate through binary fission and situate themselves in the hind gut. Metacyclic trypomastigotes are deposited on skin by defecation of the bug. They can be rubbed into wounds or mucosal surfaces. They enter cells and become amastigotes which can replicate through binary fission. Bursting of cells releases trypomastigotes which can infect new cells or bugs.
How does the trypomastigote propel itself?
By moving its flagella with energy from its kinetoplast.
What is the significance of triatomine development and when does it feed?
Feeds at night. All of the moulting stages are heamatophagous.
Other than the vector, how else is T. cruzi transmitted?
Food/fruit juice containing crushed bugs/faeces.
Sharing IV needles.
Why is it unlikely that Chaga's would be diagnosed in the acute stage of the disease?
Clinical signs aren't normally very severe so poor people are unlikely to go to a doctor.
What sort of things are seen in the acute stage?
Fever, headaches, hepatosplenomegaly, lymphadenopathy. 10% mortality
How does the inter determinate stage differ?
Only see antibodies in the blood and no circulating parasites.
What are the clinical signs of the chronic phase?
Fever, aching muscles, loss of appetite, irritability,
Cardiomyopathies (arrhythmia, cardiomegally and apical aneurisms)
Megaoesophagous and megacolon.
How is the disease diagnosed in the different stages?
Acute - blood smears, culture and xeondiagnosis.
Chronic - ELISA for antibody, PCR and IHC to detect parasite in tissues.
Why was this disease originally thought to be autoimmune?
Lack of parasite seen in the blood.
How does housing contribute to disease transmission?
Bugs hide in cracks in mud walls, thatched roofs etc. Proximity to domestic animals and wildlife also.
Best thing to do is improve housing quality.
How can insecticides be applied to control chagas?
Paint the walls/spray powdered solutions. These are often expensive and need repeat treatments.
How else can he vector transmission be prevented?
Bednets, food hygiene.
How is the infection treated?
Benznidamole & nidurtimox - these are old and have no paediatric formulations.
Why are there so few treatments?
Disease of poverty and the parasite is intracellular in immune privileged sites so it is hard to treat.
Are there any other preventative measures?
Screen pregnant women and blood donors
How has the disease migrated to Latin America?
Bugs moved due to deforestation and loss of wild food source.
Movement of migrants - baggage, blood donors
Armadillo and oposum
What triggers the immune response in the acute phase?
Parasite mucins and DNA
Which immune response clears parasites from the immune system, is there any disadvantages to this type of response?
Cellular response, however, this results in immune complex formation so there could be damage from these and excessive inflammation. The TH2 response does not decrease parasite load but there is a reduced damage due to the above.
What is chronic pathology associated with?
Increase antibody production, a TH2 response.
How might the parasite cause autoimmunity?
Bystander activation - autoreactive immune cells respond to cardiac antigens when cardiac cells are lysed by the parasite.
Cryptic epitope - antigens released are usually in too small a number or are hidden so would not have been negatively selected against during thymic development.
Molecular mimicry - the parasite has antigens similar to host antigens
Polyclonal lymphocyte activation - parasite activates lots of lymphocytes.
How does the parasite escape from the lysosome?
TcTox lyses the vacuolar membrane (it is similar to C9)