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Microbiota On Mucosal > B1- Intro To Parasitic Protozoa > Flashcards

B1- Intro To Parasitic Protozoa Flashcards

1
Q

What are Protozoa/protists

A

Microbial eukaryotes that are not fungi and can be pathogenic / have pathogenic potential

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2
Q

Why would you study them genomically

A

To study structures of other eukaryotes eg gpi anchor found first in trypanosoma

Also to study pathogenic factors they have gotten eg through lgt

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3
Q

What have multicellular life eg plants and animals derived from

A

Microbial eukaryotes (first eukaryotic lineages)

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4
Q

What was suggested by the archaezoa n hypothesis

A

That the nucleus from endogenous membranes was formed in ancestral euk before mitochondria endosymbiosis of proteobacterium

because early me shown to have no mitochondria

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5
Q

Why was this discretited

A

Even archaezoa had mt genes on genomes
Also mt-derived organelles

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6
Q

What 2 reduced mt organelles can be present in protists

A

Hydrogenosomes and mitosomes

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7
Q

What complex type of mt in eg trypanosoma

A

Kinetoplast

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8
Q

What have apicomplexa like toxoplasma gondii acquired for invasion

A

Apical organelles
3 of them
rhobtries
Micronemes
and dense granules

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9
Q

How have MICROSPORIDIA evolved mech for invasion

A

Polar tubes

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10
Q

What replaced peroxisomes for glycolysis in kinetoplasts

A

Glycosomes

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11
Q

Where did apicomplexa acquire their copy of apicoplast

A

Primary endosymbiosis of Cyanobacteria

Then red algae eukaryote was undergone secondary endosymbiosis by another euk cell

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12
Q

Give example of same but green algae

A

Euglenids

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13
Q

Which other lineage also had red algae plastid

A

Stramenopiles eg blastocystis

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14
Q

How many membranes has apicoplast got and how does it replicate

A

3

Replicates closely linked with mt (1 copy in each apixomplexan)

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15
Q

What are the 5 lineages and give examples of parasites

A

Opisthokonta- MICROSPORIDIA

Excavata - kinetoplastida eg trypanosomes

Archaeplastida

Amoebozoa - entamoeba histolytica

Sar- alveolata apicomplexa, Stramenopiles : blastocystis

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16
Q

Give 3 symbiotic relationships

A

Mutualism
Commensalism
Parasitism

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17
Q

Parasites mostly obligate symbionts but some are facultative. What does obligate mean

A

They depend on host for lifecycle so less likely to kill

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18
Q

Give example where a free living parasite can occur and infect brain

A

Naegleri fowleri

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19
Q

What’s difference between monoxenous and heteroxenous/definitive hsot

A

Need 1 host for life cycle

Need 2 or more with a definitive host for sexual maturity

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20
Q

When zoonosis occurs what are the animals said to be

A

Reservoirs for parasites eg mosquitos

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21
Q

Give 3 modes of transmission

A

Contact dependant eg dog bite, sex
Vehicle dependant eg food/water
Vector transmission: arthropod-born infections eg sandlifes , insects, mosquitos

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22
Q

Give 2 examples where infection is first gut but can disseminate to brain/cns

A

Naegleri and toxoplasma

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23
Q

Give 2 most common entamoaeba and where they reside

A

Gingivalis (oral)
Histolytica (colon)

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24
Q

How are faecal-oral gut parasites transmitted and what’s the difference between apicomplexans and rest

A

Through cysts or oocysts eg in apicomplexans

Oocysts form after sexual reproduction and produce sporozoites instead of trophozoites

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25
Q

Give some zoonoses examples of gut parasites - can happen anywhere so are more common than the ones due to hygeine

A

Cryptosporidium (originally in gorilla) , microsporidia

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26
Q

Which things can MICROSPORIDIA infect

A

Bees, fish, silk worms, humans (zoonotic)

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27
Q

What does it cause and can it become systemic

A

Chronic diarrhoea

Potentially disseminates form intestine

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28
Q

Which types form dividing spores inside parasitophorous vacuoles (enterocytozoon bieneusi doesn’t) and why mroe dangerous

A

Encephalitozoon cuniculi,intestinalis

These can disseminate eg to liver, lung or brain

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29
Q

Which divides in cytosol

A

Enterocytozoon bieneusi

30
Q

What are the main differences between toxoplasma/plasmodium and cryptosporidium

A

Crypto is monoxenous , has no mt but mitosomes instead and no apicoplast

31
Q

Are they all obligate ic or not

A

Yes they are

32
Q

Explain the hosts of toxoplasma and crypto

A

Definitive was cat (to to sexually mature)

intermediate for development is prey eg birds or rodents

Accidentally transmitted to humans

For crypto found in mammals and humans

33
Q

What are the 2 common cryptosporidium

A

Parvum (humans and other mammals)

Hominis - only humans

34
Q

Why is it life threatening

A

If someone is immunocompromosed like children = severe diarrhoea and deaths most after rotavirus

35
Q

Explain the 2 cycles from water infected (water borne) up to re infection Or transmission

A

Excysr releasing sporozoites which then infect apically the intestinal membrane and form a surface vacuole

Asexual reproduction where trophozoites form a type 1 meront (a parasitic vacuole) in which merozoites are produced

Meront released merozoites and reinfect other cells to undergo more merogony

Sexual cycle (gametogony) begins where meront 2 releases merozoites and form micro and macro gamonts, where microgametes fertilise the macro gamont to form zygote

Zygote sporulates into 4 sporozoites which

Either becomes thick occust or auto infects thin walled oocyst

36
Q

What is anthrponotic transmission in c parvum

A

Where close water supplies can infect animals from humans primarily and some strains of Parvum have adapted for human to human transmission only

37
Q

How much does toxoplasma vary in popn in commonality

A

20-75% so can be common

38
Q

Explain the entero-epithelial coccidiaj life cycle only in definitive felines

A

Ingest tissue cysts from prey eg rodents
This releases bradyzoites after excystarion by digestive enzymes which then infect intestinal si cells

Asexual merogony occurs which rupture cell releasing merozoites

Merozoites then can sexually develop into zygote through macro gamont fertilisation (only in cats)

Oocysts then sporulate (contain 4 sporozoites)

39
Q

Give example how animals or humans can then be infected through cats or their dog

A

Exposure to cat litter/faeces

From dog which bring cat litter into house

40
Q

Explain the extra-intestinal life cycle that happens in intermediate hosts infected from cat oocysts

A

Infected by the oocysts which can excyst into sporozoites which undergo merogony

These can then infect any cell but more commonly macrophages where they develop into tachyzoites (acute infection type with rapid division)

tachyzoites with rapid replication and infect any cell of the body (common in reticuloendothelial system)

Eventually encyst again due to strong th1 (tissue cysts with bradyzoites) and stay dormant eg in cns, visceral organs and muscles
(These can be transmitted to humans or cats)

Reactivated and can retransform to tachyzoites eg under immune suppression causing issues in the brain like seizures, headaches, also muscle problems like dyspnoea

41
Q

What is the only thing that can transfer to foetus

A

Tachyzoites
So if mother has an acute active infection not dormant chronic toxoplasmosis

42
Q

How can tachyzoites convert to bradyzoites which are slow replicating dormant chronic toxoplasmosis

A

In strong immune responses eg th1

43
Q

How does bradyzoites tissue cysts (common to cns/ brain/ muscle) differ to tachyzoite after periods of immunosuppression/reactivation

A

Slow replication, chronic infection,

44
Q

In chronic infection whag manifestations can occur MAINLY ONLY IF IMMUNOSUPPRESSED ASYMTOMATIC IF NOT (bradyzoites cysts are dormant but tachyzoites have acute infection symptoms)

A

Cns problems like seizures, muscular problems
Fever, dyspnoea

45
Q

What can convert bradyzoites to tachyzoites for rapid replication

A

Immunosuppression

46
Q

What sort of issues do foetuses show in congenital toxoplasmosis when acquired tachyzoites form mother

A

Microcephaly, mental retardstion, visual defects

47
Q

Which cells in eye get infected if chronic infection with toxoplasma and there is reactivation of tissue cysts and can cause necrosis / form lesions = blurred vision

A

Retinal pigment epithelium

48
Q

Why is good ifny responses of host shown to stop ocular toxoplasmosis development

A

Block replication by interfering with tryptophan pathway of parasites

49
Q

Which hla allele associated with protection from ocular toxoplasmosis

A

Hla A29

50
Q

Which protein from rhoptries in toxoplasma (some) associated with developing ocular toxoplasmosis and pathogenic potential

A

Rop16 because it downregulated rh1 responses through inducing an m2 macrophage shift (il10 is immunosuppressive)

51
Q

How many new cases of leishmania are there every year

A

1 mill

52
Q

Which arthropod vector required

A

sandflies

53
Q

Which type of leishmania is most common but name all 3

A

Cutaneous leishmaniasis - skin lesions eg ulcers

Muco-cutaneous - destruction of mucosa in mouth; nose or throat

Visceral - infect organs like spleen or liver (most deadly 95% death)

54
Q

What cell type have leishmania adapted to infect and survive/ reproduce in and what do they transition to from promastigotes injected by bite

A

Macrophages

Turn into amastigotes which multiple in macrophages

55
Q

Does this mean they are obligate ic

A

Yes

56
Q

Which skin dysbiotic increase was shown to get worse symptoms of cutaneous leishmania major infection and five specific example of how from mice models

A

Staph and streptococcus
Staph xylosis specifically can upregulste il17 responses leading to an inflammatory response and tissue damage (neutrophil recruitment)

57
Q

What is a common visceral leishmania species

A

Donovani

58
Q

How did this species show gut microbes of sandflies can affect outcome of infection/ cause dissemination to visceral organs in mice

A

Injected gut microbes aswell as the parasite and this exacerbated inflammasome NLRP3 activation of neutrophils
Via Il1b

Neutrophil recruitment was shown to induce inflammation and dissemination to eg spleen - stopped if flies took antibiotics before infection

59
Q

Which virus infects and increases parhogeneitictg of leishmania

A

Lrv1 totiviridae

60
Q

What does this induce which activates mirna Mir-155

A

Tlr3 (recognises dsrna)

61
Q

Why is this important

A

Mir-155 will activate akt/pi3k signalling which induced anti-apoptotic factors like bcl2
Mir-155 also will block apaf-1 increasing survival of mac/leishmania

And also blocks antiinflam Bcl6 (txn repressor of nfkb) which promotes an inflammatory cytokines macrophage phenotype

62
Q

Why was it suggested mt were acquired later in the phylogenetic tree of euk

A

Because early euk trichomonass and MICROSPORIDIA seemed to not have mt

63
Q

Which apical organelle is suggested to be important for forming a parasitophorous vacuole

A

Rhoptries and their contents

64
Q

Give examples of parabasalia

A

Trichomonas

65
Q

Give example of diplomonads (excavata lineage)

A

Giardia lamblia

66
Q

What adhesion proteins are released from micronemes for better attachment of apicomplexans

A

TRAP family proteins (thrombospondin related)

67
Q

Which horizontally acquired enzyme do cryptosporidium use to avoid starvation (from ifny triggered trp degradation to kyneurenine) when encapsulated above the epithelial cells and how are Microbiota related to this

A

Tryptophan synthase b

Can produce tryptophan from Indole derived from the Microbiota

68
Q

Why would a greater level of epithelial damage be seen with cryptosporidium

A

Usually immunockmpetent can intercept the merozoites after release before infecting other cells

69
Q

How is gondii commonly transmitted

A

Oocyst contaminated water/food

Tissue cysts in uncooked meat

Congenital transmission

70
Q

Like cryptosporidium , what do toxoplasma gondii form when ic so don’t come in contact eg the merozoites in macrophages

A

A parasitophorous vacuole

71
Q

What is the difference between trypanosoma brucei (gambiense and rhodensiese) and cruzi

A

Brucei is from tsetse fly and is prevalent in Africa
Cruzi is Chagas’ disease in South America

Cruzi also is intracellular vs brucei which is always extracellular (blood)

72
Q

What is the suggested Trojan horse effect of neutrophils for l.m in cutaneous leishmaniasis which can potentially explain also why neutrophil recruitment can cause Donovani dissemination to viscera

A

Suggests that they are the first hosts and shield LM before they can be uptsken by macrophages for infection

Microbiota On Mucosal (22 decks)

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