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MIMM 413 > Lecture 7 > Flashcards

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

A

t cruzi

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
Q

prevention of changas disease

A

triatomite bug is easier to eradicate from houses than mosquitos since there are fewer and less mobile
-can be pretty effective

26
Q

trypanosome cruzi life cycle

A

-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
Q

true or false: trypomastigote replicate

A

nah they don’t

28
Q

true or false: only amastigotes are released from infected cells

A

false also trypomastigotes

29
Q

mode of entry of cruzi

A

-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
Q

what does chagas disease cause

A

-takes 50-60 years to fuck you up and you get hearts disease
-darwin died of it

31
Q

chagas disease clinical evolution

A

-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
Q

chagas acute disease

A

-acute phase: positive smear, positive culture, positive pcr results

33
Q

chagas chronic phase

A

-chronic phase: negative smear, positive pcr 20-70% of people, diagnosis based on serologic results

34
Q

diagnosis of chagas disease

A

pcr
giemsa (acute phase)
serology/pcr (chronic phase)

35
Q

treatment of chagas disease

A

benznidazole for acute and chronic phase

36
Q

what is ised to kill triatomines

A

deltamethrin

37
Q

t cruzi amastigote infects which cells

A

often in heart muscle cells
-looses actin filaments
-sarcomere (made of myosin/actin)

38
Q

what are the cruzi surface proteins

A

-mucin proteins that are heavily glycosylated

39
Q

t cruzi surface trans sialidase

A

provides sialic acid for mucin

40
Q

insect epimastigote/trypomastigote mucins

A

-short mucin non-variable
-protection from insect gut enzyme
-coats parasite with carbohydrate layer

41
Q

mammalian amastigote/trypomastigote mucin

A

-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
Q
A

MIMM 413 (24 decks)

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