Lecture 7 Flashcards
true or false: kinetoplastida include trypanosomes and leish
true
which trypanosome is only in humans and not animals
trypanosome gambiense
trypanosome brucei life cycle
-tsetse fly takes blood meal
-injected metacyclic trypomastigotes transform into bloodstream trypomastigotes which are carried to other sites
-trypanosomes multiply by binary fission in various body fluids like blood, lymph
-trypomastigotes in blood
-fly takes a meal
-bloodstream trypomastigotes transform into procyclic trypomastogotes in tsetse fly’s midgut, they multiply by binary fission
-procyclic trypomastigotes leave the midgut and transform into epimastigotes
-epimastigotes multiply in salivary glands, they tansform into metacyclic trypomastigotes
how can a pathogen replicate in the blood against the antibody response
-adcc: antibody dependant cellular cytotoxicity
-cdc: complement dependent cytotoxicity
-mac: membrane attachment complement
what is vsg
-variant surface glycoproteins
-coats the surface of the body, flagellum and also some vesicles
what is the VSG made up of
-exposed variable region
-non-exposed conserved region
-gpi anchor which anchors to the lipid membrane
what is quirky about vsg
-as the body makes antibodies the parasite switches the surface glycoproteins
how does vsg switching occur: more like what is on the dna
-dna sequencing of genome has identified hundreds of vsg genes on numerous chromosomes
-each gene with different variable regions sequence, and identical signal, conserved and GPI insertion anchor region for insertion into lipid bilayer
expression of different by which polymerase
-rna pol normally expresses ribosomal rna, the most abundant rna in the cell
-only one telomeric located vsg is expressed at a time
true or false: vsg switching is pre-programmed in genome
true
which polymerase transcripts internal gene of trypanosomes
pol 2
-there is trans splicing using mini exon transcript
-basically trans splicing is the only way to seperate the genes dur to polycistronic pre-mrna
true or false: leish/trypanosomes have polycostronic genes
true
kinetoplasts are specific to what
trypanosomes and leish
leish and trypanosome rna editing
-there are maxi circle which sucks and has a lot of mistakes so basically you get no good proteins
-the mini circle contains a guide rna and it hybridizes with the shit dna
-the remplate will carry out the editing
-usually you get uridine insertion or deletion
what does trypanosome cruzi cause
chagas disease
who found chagas disease
-carlos changas found the parasite in the triatomite bug
changas disease is caused by what
triatomine bug it bites people
who was the first changas disease
berenice she had the same parasite
evolution of trypanosome: hos did they get from africa to south america
continental drift, before they were all attached to eachother before, 200 million years ago
which strains of trypanosomes for which continent
-brucei: africa
-cruzi: south america
-sp (kangaroo): australia
true or false: trypanosomes were present long before humans
true: 200 million years
-30 000 ys americas T cruzi
-85 000 yrs africans T brucei
which trypanosome strain has a bigger kinetoplast
t cruzi
changas disease in north america
-can: less than 0.1 million
-us: between 0.3 and 1 million
-mexico: 1-6 million cases
transmission of changas disease
-transmits in cats, bug bites cat, bites humans, bites carcajou
prevention of changas disease
triatomite bug is easier to eradicate from houses than mosquitos since there are fewer and less mobile
-can be pretty effective
trypanosome cruzi life cycle
-bite
-amastigote replicates in muscle cells
-goes to trypomastigote in megaesophagus, megacolon and cardiomyopathy
-bug bite get tryponmastigote
-gets into epimastigote
-gets into trypomastigote
true or false: trypomastigote replicate
nah they don’t
true or false: only amastigotes are released from infected cells
false also trypomastigotes
mode of entry of cruzi
-trypomastigote damage to membrane: damage to cell membrane causes ca2+ influc
-flagella drives entry: ca2+ influx recruits lysosomes to repare damage
-lysosome repair membrane: remodeling of plasma membrane during repair allows entry allows entry of T.Cruzi
what does chagas disease cause
-takes 50-60 years to fuck you up and you get hearts disease
-darwin died of it
chagas disease clinical evolution
-bite
-1-2 weeks
-acute phase: positive smear, positive culture, positive pcr results
-chronic phase: negative smear, positive pcr 20-70% of people, diagnosis based on serologic results
-chronic phase: 70-80% of infected people will have the inderterminate form throughout their lives
-20-30% will have the disease progression over years and decades: determinate form chagas cardiomyopathy or chagas gastrointestinal or both
chagas acute disease
-acute phase: positive smear, positive culture, positive pcr results
chagas chronic phase
-chronic phase: negative smear, positive pcr 20-70% of people, diagnosis based on serologic results
diagnosis of chagas disease
pcr
giemsa (acute phase)
serology/pcr (chronic phase)
treatment of chagas disease
benznidazole for acute and chronic phase
what is ised to kill triatomines
deltamethrin
t cruzi amastigote infects which cells
often in heart muscle cells
-looses actin filaments
-sarcomere (made of myosin/actin)
what are the cruzi surface proteins
-mucin proteins that are heavily glycosylated
t cruzi surface trans sialidase
provides sialic acid for mucin
insect epimastigote/trypomastigote mucins
-short mucin non-variable
-protection from insect gut enzyme
-coats parasite with carbohydrate layer
mammalian amastigote/trypomastigote mucin
-long mucin group 1: hyper variable N-terminal
-long mucin group 2, variable core
-being shed into the bloood acting as decoys
-for immune evasion
