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BIOL314: Parasitology > Lecture 6: Toxoplama gondii > Flashcards

Lecture 6: Toxoplama gondii Flashcards

1
Q

True or false: T. gondii is an obligate extracellular pathogen?

A

False: it is an obligate intracellular pathogen

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2
Q

What phylum does T. gondii belong to?

A

Apicomplexa

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3
Q

What is the typical infective route for T. gondii?

A

oral

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4
Q

What disease does T. gondii cause?

A

Toxoplamosis

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5
Q

What is the end stage host of T. gondii?

A

warm blooded animals

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6
Q

What type of reproduction occurs in end stage hosts of T. gondii?

A

asexual reproduction only

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7
Q

What is the definitive host of T. gondii and what type of replication occurs here?

A

Cat

sexual reproduction

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8
Q

How is it that so many people are infected with T. gondii but not continuously ill?

A

Immune system controls infection - survives as a latent infection in the form of tissue cysts (such as brain)

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9
Q

How is toxoplasmosis transmitted?

A
  • foodborne (undercooked meat)
  • zoonosis (Cat litter trays)
  • congenital (mother to child)
  • transplantation
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10
Q

Under what conditions may toxoplasmosis cause serious complications?

A

in immunocompromised individuals (infants, elderly, HIV, immunosuppressed - cancer therapy, transplant)

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11
Q

What are the main symptoms following toxoplasmosis infection?

A

transient intestinal inflammation
flu-like symptoms

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12
Q

What is congenital toxoplasmosis and give three effects this can have on the foetus?

A

infection with toxoplasmosis during pregnancy that is transmitted to foetus

can result in hydrocephalus, epilepsy. hearing loss, learning disabilities, cerebral palsy

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13
Q

What is ocular toxoplasmosis?

A

cysts at the back of the eye can result in blurred vision, floaters, loss of vision

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14
Q

What is the most serious toxoplasmosis infection?

A

cerebral toxoplasmosis where cysts in brain but the infection is not controlled and can result in immune response and inflammation (serious and life-threatening as can result in confusion, seizures, loss of co-ordination)

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15
Q

Describe the life cycle of T. gondii

A

Tissue cysts contain bradyzoites
- in definitive cat host, the bradyzoites can differentiate into merozoites and allow sexual reproduction to produce gametocytes that form a zygote or differentiate into tachyzoites as part of asexual reproduction
- zygotes form oocysts that contain sporozoites

bradyzoites (from ingested cysts) and sporozoites (from ingested oocysts) differentiate into highly infective tachyzoites as part of the asexual reproductive cycle in the end-stage host
- tachyzoites invade cells and multiply until cell dies releasing more tachyzoites
- tachyzoites then differentiate back into bradyzoites and form cysts mainly in the brain, liver and muscle

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16
Q

how can an end-stage host become infected?

A
  • ingesting oocysts containing sporozoites from cat faeces (sporozoites invade tissues and develop into tachyzoites then bradyzoites in cysts)
  • ingesting meat infected with bradyzoite cysts (bradyzoites differentiate into tachyzoites)
17
Q

How do we respond to T. gondii infection?

A

once recognition occurs, two key cytokines are produced:
IL-12 (produced by innate immune cell responses that trigger the activation of the adaptive immune response) and INF-gamma (produced by the adaptive immune cells)

18
Q

how do we recognise T. gondii infection?

A

PRRs recognise PAMPs
- TLR1/2 and 4 potentially recognise GPI anchor of parasite
- once within the cell, TLR7 and TL9 potentially recognise RNA and DNA, respectively
- TLR11 and TLR12 recognise profilin during parasitophorous vacuole

19
Q

Give two examples of transmembrane PRRs and two examples of Cytosolic PRRs

A

Transmembrane:
- TLRs (plasma membrane or endosomes)
- C-type lectin receptors (CTLs)

Cytosolic:
- Nod-like receptors (NLRs)
- RIG-1 like receptors (RLRs)

20
Q

What is profilin, how is it recognised by our immune system?

A

Profilin is an actin binding protein in the parasite that is essential for motility and cellular invasion

recognised by TLR11 and TLR12

21
Q

What is the significance of MyD88 in innate recognition of the parasite?

A

all the TLRs involved in recognition of T. gondii activate signalling pathways that all involve the protein MyD88 that ultimately activates transcription of IL-12
- k/o MyD88 mice fail to produce IL-12 and are susceptible to infection

22
Q

What is the significance of UNC93B1 in innate recognition of the parasite?

A

UNC93B1 is attached to the N-terminal region of TLR7, 9, 11, and 12 (but not TLR1,2, or 4) and involved in signalling for these TLRs.
- k/o UNC93B1 mice are highly susceptible to infection

This indicates that perhaps the recognition of the GPR anchor by TLR1/2 and 4 is not as important in parasite recognition (not enough to produce effective immune response alone when the other TLRs are non-functional due to UNC93B1 k/o)

23
Q

which cell does the innate recognition and IL-12 production largely occur in?

A

CD8 alpha dendritic cells

24
Q

What does IL-12 do?

A

signals to naive helper CD4 T cells to drive the T-helper 1 response to make IFN-gamma
- Th1 response is good for intracellular parasites

25
Q

What other immune cell is essential in the production of IFN-gamma?

A

NK cells

26
Q

How does IFN-gamma result in parasite killing in immune cells?

A

Immune cells such as monocytes and macrophages that have phagocytosed parasites have IFN-gamma receptor
- binding of IFN-gamma to receptor results in STAT1 activation and toxicity-inducible reactive oxygen species and nitric oxide molecules that damage the parasitophorous vacuole
- STAT1 signalling also results in activation of GTPases (IRGs) and p67 guanylate-binding proteins (GBPs) that rupture the parasitophorous vacuole

26
Q

How does IFN-gamma result in parasite killing in non-immune cells?

A

IFN-gamma receptor activation results in STAT1 signalling that results in activation of GTPases (IRGs) and p67 guanylate-binding proteins (GBPs) that rupture the parasitophorous vacuole

27
Q

What is one of the big problems between the mouse model (from which a lot of the information about T. gondii infection has been found) and humans?

A

Humans have 3 stop codons on the TLR 11 gene and a complete absence of the TLR 12 gene = no ability to recognise profilin as a human

28
Q

What is different about the human equivalent of the CD8alpha dendritic cells in mice?

A

The main human producers of IL-12 are the opposite dendritic cell population to that of the mouse model (i.e. the human equivalent of the mouse non-CD8alpha DCs)

28
Q

How do human dendritic cells recognise the live parasites?

A

phagocytosis of the parasite possibly sensed by cytosolic PRRs such as RIG-1

28
Q

How do infected rats/mice behave different around cat urine?

A

When infected, they lose their aversion to cat urine (which would normally promote their survival)
- parasite knows it is in an end stage host because it doesn’t have sexual reproduction
- to promote sexual reproduction and carry on the parasite lifecycle, it makes the mouse more likely to take risks and get killed by the cat

29
Q

Describe the host cell invasion and manipulation by T. gondii

A
  • actin-based motility and protein secretion from the Rhoptory bulb allows envagination to create a parasitophorous vacuole
  • the protein secretion recruits mitochondria and host ER and avoids fusion with lysosomes and endosomes
  • activation of anti-inflammatory pathways such as STAT3/6 (opposite of STAT1) and SOCS3
  • GTPase inhibitors prevents non-immune cell breakdown of the parasite wall via STAT1 IFN-gamma signalling
30
Q

A small study showed a significant correlation between toxoplasmosis infected humans and what type of behaviour?

A

risk-taking behaviour (although large studies have suggested this is unlikely in humans - although very clear in rats/mice)

31
Q

Give two human diseases that toxoplasmosis infection has been linked to

A

Alzheimer’s disease
Schizophrenia

BIOL314: Parasitology (10 decks)

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