Lecture 7 Flashcards

1
Q

true or false: kinetoplastida include trypanosomes and leish

A

true

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2
Q

which trypanosome is only in humans and not animals

A

trypanosome gambiense

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3
Q

trypanosome brucei life cycle

A

-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

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4
Q

how can a pathogen replicate in the blood against the antibody response

A

-adcc: antibody dependant cellular cytotoxicity
-cdc: complement dependent cytotoxicity
-mac: membrane attachment complement

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5
Q

what is vsg

A

-variant surface glycoproteins
-coats the surface of the body, flagellum and also some vesicles

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6
Q

what is the VSG made up of

A

-exposed variable region
-non-exposed conserved region
-gpi anchor which anchors to the lipid membrane

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7
Q

what is quirky about vsg

A

-as the body makes antibodies the parasite switches the surface glycoproteins

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8
Q

how does vsg switching occur: more like what is on the dna

A

-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

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9
Q

expression of different by which polymerase

A

-rna pol normally expresses ribosomal rna, the most abundant rna in the cell
-only one telomeric located vsg is expressed at a time

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10
Q

true or false: vsg switching is pre-programmed in genome

A

true

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11
Q

which polymerase transcripts internal gene of trypanosomes

A

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

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12
Q

true or false: leish/trypanosomes have polycostronic genes

A

true

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13
Q

kinetoplasts are specific to what

A

trypanosomes and leish

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14
Q

leish and trypanosome rna editing

A

-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

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15
Q

what does trypanosome cruzi cause

A

chagas disease

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16
Q

who found chagas disease

A

-carlos changas found the parasite in the triatomite bug

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17
Q

changas disease is caused by what

A

triatomine bug it bites people

18
Q

who was the first changas disease

A

berenice she had the same parasite

19
Q

evolution of trypanosome: hos did they get from africa to south america

A

continental drift, before they were all attached to eachother before, 200 million years ago

20
Q

which strains of trypanosomes for which continent

A

-brucei: africa
-cruzi: south america
-sp (kangaroo): australia

21
Q

true or false: trypanosomes were present long before humans

A

true: 200 million years
-30 000 ys americas T cruzi
-85 000 yrs africans T brucei

22
Q

which trypanosome strain has a bigger kinetoplast

23
Q

changas disease in north america

A

-can: less than 0.1 million
-us: between 0.3 and 1 million
-mexico: 1-6 million cases

24
Q

transmission of changas disease

A

-transmits in cats, bug bites cat, bites humans, bites carcajou

25
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
26
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
27
true or false: trypomastigote replicate
nah they don't
28
true or false: only amastigotes are released from infected cells
false also trypomastigotes
29
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
30
what does chagas disease cause
-takes 50-60 years to fuck you up and you get hearts disease -darwin died of it
31
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
32
chagas acute disease
-acute phase: positive smear, positive culture, positive pcr results
33
chagas chronic phase
-chronic phase: negative smear, positive pcr 20-70% of people, diagnosis based on serologic results
34
diagnosis of chagas disease
pcr giemsa (acute phase) serology/pcr (chronic phase)
35
treatment of chagas disease
benznidazole for acute and chronic phase
36
what is ised to kill triatomines
deltamethrin
37
t cruzi amastigote infects which cells
often in heart muscle cells -looses actin filaments -sarcomere (made of myosin/actin)
38
what are the cruzi surface proteins
-mucin proteins that are heavily glycosylated
39
t cruzi surface trans sialidase
provides sialic acid for mucin
40
insect epimastigote/trypomastigote mucins
-short mucin non-variable -protection from insect gut enzyme -coats parasite with carbohydrate layer
41
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
42