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Parasitology > Week 7 > Flashcards

Week 7 Flashcards

1
Q

leishmania evolution

A

phylogenetic tree organization suggests the different types of diseases caused evolved first and then they split geographically

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2
Q

dangers to the leishmania parasite

A
  • when the promastigote binds to a macrophage, it creates ROS
  • inside the lysosome they have to deal with acidification and digestion
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3
Q

what is the survival strategy of leishmania?

A
  • not to be in the blood too long and to enter macrophages
  • they also produce proteins that cleaves compliments off of itself in the blood so it doesn’t get opsonized or sequestered
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4
Q

what happens to the leishmania promastigote once it is phagocystosed

A
  • loses its flagellum and becomes an amastigote
  • this signals it to move on to the next stage in the life cycle
  • wants to be phagocytosed and uses the host immune system against it
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5
Q

how do the leishmania promastigotes deal with the ROS?

A
  1. Physical barrier:
    - has a protective lipophosphoglycan coat (LPG)
  2. Down-regulation:
    - LPG coat interferes with signal transduction pathways
    - Inhibits protein kinase C, which normally triggers the respiratory burst (creation of ROS)
  3. Detoxification with antioxidant enzymes
    - get rid of any ROS that managed to get made
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6
Q

how do kinetoplasts deal with the ROS

A
  • lack catalase and thioredoxin
    reductase (enzymes that deal with ROS)
  • use NADPH to reduce the ROS
  • use the trypanothione pathway
  • kinetoplast specific and
    contains two molecules of glutathione linked by a polyamine (spermidine)
  • this pathway is a good drug target because it is unique to kinetoplasts
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7
Q

how does leishmania deal with the acidification and digestion in lysosomes?

A
  1. Resistance to hydrolytic enzymes
    - have surface glycoproteins refractory to host lysosomal enzyme activity
    - probably so coated in sugars that the enzymes can’t get access to the amino acid backbone
  2. Enzymatic destruction
    - Surface proteins also destroy host enzymes
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8
Q

what is weird about trypanosome transcription?

A
  1. Seems to be very little regulation at the PolII promoter level
    - Coding sequence levels controlled by maturation and stability of mRNAs
    - they make all mRNAs, then degrade the ones they don’t want
  2. Genes are transcribed as polycistronic messages
    - 1 giant mRNA molecule with many unrelated genes on it
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9
Q

Polycistronic transcription

A
  • use polycistronic transcription to transcribe multiple protein-coding genes as a single pre-mRNA transcript
  • single RNA polymerase II transcribes the entire gene cluster into a large polycistronic pre-mRNA starting from the transcription start site (TSS) and extends in both directions
  • ends at transcription termination site (TTS)
  • splicing then occurs to add spliced leader and poly A tail to each mRNA
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10
Q

Base J

A
  • Trypanosomes have another base
  • hypermodified thymidine
  • acts as an RNA PolII terminator in
    most trypanosomes
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11
Q

RNA sequencing in transcription of trypanosomes

A
  • technique to see what genes are transcribed
    and at what level
    in host cells:
  • oligo dT to isolate only mRNA
  • stretch of T’s bind to the poly A tail
    in parasite:
  • can use sequence complementary to SL to isolate the mRNA that is from the parasite for sequencing
  • could combine to look at host and parasite mRNA from the same sample
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12
Q

how do we distinguish between the different life stages of T. brucei?

A
  • Kinetoplast localization: Location of kinetoplast varies in development
  • length of flagellum also varies
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12
Q

slender vs stumpy trypomastigotes

A

slender:
- initial phase of infection
- metabolically active
- replicating
stumpy
- after replication
- cannot divide
- less metabolically active
- turns stumpy when there is enough density of slender form in the blood

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13
Q

Quorum sensing

A
  • cell-to-cell communication mechanism used by bacteria to coordinate collective behaviors based on their population density
  • done to switch between slender and stumpy trypomastigotes
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14
Q

quorum sensing in trypanosomes

A
  • make public goods to determine density, something all trypanosomes in can blood stream can see
  • slender releases peptidases that degrade host and parasite proteins in the bloodstream
  • creates oligopeptides (little chunks of protein)
  • the more trypanosomes there are, the more peptidases present and the more oligopeptides
  • the trypanosomes have a protein that actively transports oligopeptides back into the parasite, once there are enough present it will turn stumpy
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15
Q

what determines the geographic distribution of Trypanosomes?

A

vector determines endemic
regions for each parasite

16
Q

Risk factors for Trypanosome diseases

A
  1. all common risk factors for NTDs
    - Rural life, and activities that expose people to tsetse flies
    - lack of health care
  2. Cattle are resevoirs
    - catlle movements can carry endemics with them
  3. Civil unrest
17
Q

Trypanosome infection

A
  • transmitted by tsetse flies
  • they are pool feeders: bites then feed on blood that pools
  • First indication is painful reaction at the site of the bite
  • have 4 phases
18
Q

Phase 1 of trypanosome infection

A
  • lasts 1-2 weeks
  • incubating in skin, hasn’t moved to blood
19
Q

Phase 2 of trypanosome infection

A
  • parasites enter the circulation (trypomastigote phase)
  • Variable duration.
  • Headache, malaise, rash
  • Tryps start reproducing rapidly and enter the lymphatic system
  • Parasitemias (level of parasite in the blood) can be high
20
Q

Phase 3 of trypanosome infection

A
  • parasites collect in the lymph nodes
  • Fever, headache, weakness, delayed pain sensation
  • can last months or years (depends on type)
  • Winterbottom’s sign: Enlargement of lymph nodes in the cervical
    triangle on the back of the neck
  • B cell recruitment leads to lymph node enlargement and trypanosome lysis
  • Recurrent fever every 7-10 days
21
Q

Phase 4 of trypanosome infection

A
  • CNS infection
  • Headaches are severe, emaciation, apathy, drowsiness and coma, death
  • fatal if untreated
  • Interferes with circadian rhythms
  • biological clock altered
  • Inflammation leads to demyelination
22
Q

Diagnosis of trypanosome infection

A
  • Concentrate blood and look via microscope
  • Serology (blood test) – antibodies, high levels of IgM common
23
Q

Treatment of trypanosome infection

A
  • Drugs are old, dangerous, and difficult to administer
  • Drug resistance is increasing
  • high fatality rate
  • expensive treatment
24
Q

Trypanotolerance in N’Dama cows

A
  • some breeds of cows can tolerate trypanosomes
  • you would figure out what genes are responsible through cross breeding experiments, followed by genome wide analysis
  • Includes both resistance (less parasites) and tolerance (less anemia)
  • complex trait
25
Q

What are the 3 routes host animals have to lower disease?

A
  1. Avoidance:
    - less exposure
  2. Resistance
    - immune control of parasite number
    - lower parasitemia, get less parasites when infected
  3. Tolerance:
    - reduce the effects of pathogen burden
    - have same # of parasites, just less affected
26
Q

Splice leader (SL)

A
  • added to mature mRNAs in polycistronic transcription
  • 5’ capping structure
  • there are hundreds of copies of the SL gene
  • they each have a promoter and are transcribed similar to our genes

Parasitology (12 decks)

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