Triatomines and T cruzi interactions Flashcards
Describe the lifecycle of T cruzi.
Trypomastigotes in faeces –> enter through a wound or mucosal membrane –> invade cells (particularly intestinal epithelia) –> differentiate into intracellular amastigotes and multiply –> differentiate back into trypomastigotes and released into the bloodstream when pseudocysts rupture–> Trypomastigotes infect cells and transform into intracellular amastigotes –> can be taken up by bugs and differentiate into epimastigotes –> multiply in the midgut and transform into metacyclic trypomastigotes in the hindgut –> infect human
What are acute symptoms of chagas?
Fatigue, malaise, spleen and lymph enlargement= non specific acute symptoms.
Romanas sign and chagoma = more specific acute symptoms.
What chronic symptoms do less than 1% of patients develop?
BOTH conductivity failure in heart and congestive heart failure.
What increases the risk of congenital transmission?
Parasites in the bloodstream during pregnancy.
Why is xenodiagnosis sometimes better than PCR?
SOmehow act like filters for the parasites and can pick up v low parasitemias where PCR may not. PCR can sometimes be as low as 20% sensitive.
How is chagas treated? What are the problems with this?
Benznidazole and nifurtimox. Side effects get worse with patient age (best prognosis if treated within the first year of life).
How efficient is transmission of T cruzi?
May require 4000 infective faecal events
What are the predominant vectors in:
- The southern cone
- Northern South America (above Amazon basin)
- Central America
- SC: T infestans (1˚), P megistus (2˚)
- Amazon basin: R prolixus
- Central: T dimidiata
How many nymphal stages of triatomines are there and what do they require for progression to the next stage?
- Each stage blood feeds.
What are reservoirs for T cruzi in the US and why are there limited cases?
Opossums, raccoons, bats and rodents etc are reservoirs.
Limited cases as although 5 of the 12 species present in the US can be routinely infected with T cruzi, itis very sylvatic and distribution limits the disease (people aren’t exposed very much).
Why is it impossible for T cruzi to be eliminated or eradicated?
Impossible due to the huge sylvatic reservoirs. Almost any mammal can be fed on by triatomines and be infected with T cruzi. AS vector control is not sustained, reinfestation occurs from peridomestic triatomines which have exited buildings post IRS.
How can opossums be both a vector and a reservoir?
Secrete trypomastigotes through their scent glands which other opossums can come and lick, thereby making them both the vector and the reservoir.
Why is maintained vector control needed?
- To prevent reinfestation from peridomestic populations that have exited households
- Long lifecycle ~1 year from egg to nymph so need to maintain good control to eliminate
WHich lineage is associated most with human infection?
TC1- heavily associated with opossums. Causes heart disease.
What are the differences between T cruzi lineages?
Huge genetic diversity (even more so than between species of other things?) Are associated with different mammalian hosts, vectors, ecological niches and pathological presentation.
