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Summer Course II > Parasitology > Flashcards

Parasitology Flashcards

1
Q

Why are animal models especially important for the study of parasitic disease?

A

Parasites depend on a host -> in vitro culture is difficult/impossible

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2
Q

Why is it especially hard to develop good model systems for parasites?

A

Complex life cycles of parasites require multiple types of interaction

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3
Q

Why is it easier to develop model systems for protozoic parasites than for helminths?

A

Protozoa share a lot of characteristics with bacteria and are capable of asexual reproduction, whereas helminths require sexual reproduction in a host

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4
Q

Why does the sexual reproduction of helminths make them extra difficult to study?

A

No clonal population -> higher variation = difficult to study

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5
Q

Which two life cycle stages does Giardia lambia have, and where can they be found?

A
  1. Cyst -> infective stage, found in the external environment
  2. Trophozoite -> replicating stage, found in the intestinal gut
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6
Q

How does Giardia lamblia replicate?

A

Asexual replication by division

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7
Q

With how many and which cell types does Giardia lamblia interact in the intestinal gut

A

One cell type -> gut epithelial cells

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8
Q

Why is it relatively easy to culture Giardia lamblia?

A

Both the external & intestinal environment can be easily mimicked

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9
Q

High quality genome sequencing of Giardia lamblia [is/isn’t] available

A

High quality genomes are available

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10
Q

Which aspects of Giardia lamblia are often studied using model systems? (2)

A
  1. Host-pathogen interaction for different genotypes
  2. Transmission dynamics
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11
Q

How can trypanosomes be cultured?

A

By mimicking the various environments they require for their life cycle stages

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12
Q

Which life cycle stages of trypanosomes can be cultured?

A
  1. Procyclics
  2. Epimastigotes
  3. Long slender form
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13
Q

What is the disadvantage of culturing trypanosomes in a culture system mimicking a particular environment?

A

Parasites adapt to in vivo culture and often have monomorphic development -> no differentiation to further life cycle stages

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14
Q

How can one validate results obtained from monomorphic trypanosome cultures

A

By using fresh isolates to compare the results to

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15
Q

Genetic manipulation techniques for trypanosomes [are/aren’t] available

A

Genetic manipulation techniques are available

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16
Q

Which three types of genetic manipulation are commonly performed in trypanosomes?

A
  1. Overexpression
  2. RNA interference
  3. Knock-out
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17
Q

What kind of studies are often performed using trypanosome culture systems? (4)

A
  1. Antigenic variation
  2. RNA editing
  3. Kinetoplast DNA replication
  4. Host tissue invasion
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18
Q

Which two Leishmania life cycle stages can be cultured?

A
  1. Promastigotes = insect form
  2. Amastigotes = mammalian form
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19
Q

In which conditions can Leishmania amastigotes be cultured?

A

Mammalian cell lines

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20
Q

What is the disadvantage of culturing Leishmania in specific promastigote or amastigote media?

A

Monomorphic development

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21
Q

What kind of medium has to be used to culture Leishmania amastigotes, and why?

A

Acidic medium -> mimics conditions in phagosomes, where they usually reside

22
Q

How can Leishmania host-pathogen interaction studies be performed?

A

Culturing them in phagocytic cell lines

23
Q

Why is it impossible to culture Plasmodium spp. or develop a good animal model?

A

Their large number of developmental stages cannot be replicated in the lab, and animal models aren’t representative for malaria tropica

24
Q

Why are animal models for malaria tropica not representative?

A

Organ failure due to sequestering of red blood cells does not occur

25
Q

How can malaria infections still be studied, despite the lack of a good animal model?

A

Controlled human malaria infections

26
Q

Which Plasmodium life cycle stage is the main vaccine target, and why?

A

Sporozoite stage = stage injected by mosquitos -> extracellular stage, exposed to the immune system

27
Q

What type of vaccines are being developed for malaria? Why is this type advantageous?

A

Live attenuated vaccines -> parasites go through multiple life cycle stages, resulting in immunity against several stages

28
Q

What is a possible alternative malaria vaccine strategy (alternative to sporozoite stage)? Why?

A

Targeting gametocytes = mosquito stage
The parasite is very vulnerable at this stage; by inducing antibodies against this stage that get taken up with the blood meal, development of the parasite in the mosquito can be prevented

29
Q

What kind of vaccine strategy can Plasmodium gametocyte vaccines be used for? What is the problem with this kind of vaccines?

A

Transmission-blocking vaccines
Problem: benefit for the vaccinated person is limited -> does not protect against disease

30
Q

To which class does Ascaris lumbricoides belong?

A

Nematodes = roundworms

31
Q

Which stages of Ascaris lumbricoides development can be resembled in a monoculture system?

A

A model system based on isolated eggs from stool:
1. Culturing & hatching of eggs
2. Culturing of larvae

32
Q

How can the adult stage of Ascaris lumbricoides development be modelled?

A

Animal model: Ascaris suum infection in pigs

33
Q

There [are/aren’t] genetic manipulation techniques available for Ascaris lumbricoides

A

Aren’t

34
Q

To which class do schistosomes belong?

A

Trematodes = flatworms

35
Q

What aspect of schistosomiasis is most often studied? Why?

A

Interaction with host immune system
Parasite can survve for years within host

36
Q

In vitro models for schistosomiasis [are/aren’t] available

A

No in vitro models available -> only animal models

37
Q

What kind of animal models are used to mimic schistosomiasis?

A

Two-stage animal model, encompassing a snail and mammalian phase

38
Q

Which animals are most often used in model systems of the mammalian phase of schistosomiasis? (2)

A
  1. Mice
  2. Hamster
39
Q

What are the differences between animal models and human infections of schistosomiasis? (5)

A
  1. Parasite load
  2. Life span of infections
  3. Life span of hosts
  4. Infection/exposure
  5. Host genetics
40
Q

Why is the parasite load in animal models of schistosomiasis very different from human infections?

A

Amount of worm pairs/kg of body weight in animals is far higher than in humans

41
Q

What is the life span of schistosomiasis infections in animal models vs. in humans?

A

Animal models rapidly clear the infection (~6 weeks), whereas humans become chornically infected (~10 years)

42
Q

What is the limitation caused by the limited life span of model animals used in schistosomiasis models?

A

Animals don’t live long enough to accurately mimic chronic human infections

43
Q

What is the difference in exposure/infection between animal models of schistosomiasis and human infections?

A

Animals are exposed to a single dose of high numbers of parasites, whereas humans frequently have chronic exposure to lower numbers

44
Q

What is the difference in host genetics between animal models of schistosomiasis and human infections?

A

Animals are genetically homogenous, whereas humans suffering from infection is heterogenous

45
Q

What is the average lifespan of schistosomes in animal models?

A

~6 weeks

46
Q

Rats are immune to schistosomiasis infections, but are still studied. Why?

A

Difference to mice/hamsters can be studied to inform possible resistance mechanisms to schistosomiasis

47
Q

What knowledge about schistosomiasis has been obtained through animal models? (6)

A
  1. Immune status of host does not affect parasite development
  2. Egg excretion is dependent on host immune system
  3. Pathology studies for granuloma formation/fibrosis
  4. Egg production & excretion studies
  5. Immune modulating factors excreted by eggs
  6. Parasitic factors that inhibit thrombosis
48
Q

Immunosuppression causes [lower/higher] schistosome egg excretion

A

Lower -> immune system is necessary to free eggs from tissues to be excreted

49
Q

Which immune modulating factors are excreted by schistosome eggs? (2)

A
  1. Omega 1 -> drives Th2-response
  2. IPSE/alpha-1 -> involved in granuloma formation
50
Q

How does Omega 1 excreted by schistosome eggs drive Th2-responses?

A

T2 ribonuclease -> RNAse that interferes with mRNA signaling, driving DCs to a Th2-type

51
Q

Why is discovery of schistosome factors that inhibit thrombosis useful?

A

Possibly allows for drug discovery of new anticoagulants

Summer Course II (4 decks)

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