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

B1- Intro To Parasitic Protozoa Flashcards

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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
Give some zoonoses examples of gut parasites - can happen anywhere so are more common than the ones due to hygeine
Cryptosporidium (originally in gorilla) , microsporidia
26
Which things can MICROSPORIDIA infect
Bees, fish, silk worms, humans (zoonotic)
27
What does it cause and can it become systemic
Chronic diarrhoea Potentially disseminates form intestine
28
Which types form dividing spores inside parasitophorous vacuoles (enterocytozoon bieneusi doesn’t) and why mroe dangerous
Encephalitozoon cuniculi,intestinalis These can disseminate eg to liver, lung or brain
29
Which divides in cytosol
Enterocytozoon bieneusi
30
What are the main differences between toxoplasma/plasmodium and cryptosporidium
Crypto is monoxenous , has no mt but mitosomes instead and no apicoplast
31
Are they all obligate ic or not
Yes they are
32
Explain the hosts of toxoplasma and crypto
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
What are the 2 common cryptosporidium
Parvum (humans and other mammals) Hominis - only humans
34
Why is it life threatening
If someone is immunocompromosed like children = severe diarrhoea and deaths most after rotavirus
35
Explain the 2 cycles from water infected (water borne) up to re infection Or transmission
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
What is anthrponotic transmission in c parvum
Where close water supplies can infect animals from humans primarily and some strains of Parvum have adapted for human to human transmission only
37
How much does toxoplasma vary in popn in commonality
20-75% so can be common
38
Explain the entero-epithelial coccidiaj life cycle only in definitive felines
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
Give example how animals or humans can then be infected through cats or their dog
Exposure to cat litter/faeces From dog which bring cat litter into house
40
Explain the extra-intestinal life cycle that happens in intermediate hosts infected from cat oocysts
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
What is the only thing that can transfer to foetus
Tachyzoites So if mother has an acute active infection not dormant chronic toxoplasmosis
42
How can tachyzoites convert to bradyzoites which are slow replicating dormant chronic toxoplasmosis
In strong immune responses eg th1
43
How does bradyzoites tissue cysts (common to cns/ brain/ muscle) differ to tachyzoite after periods of immunosuppression/reactivation
Slow replication, chronic infection,
44
In chronic infection whag manifestations can occur MAINLY ONLY IF IMMUNOSUPPRESSED ASYMTOMATIC IF NOT (bradyzoites cysts are dormant but tachyzoites have acute infection symptoms)
Cns problems like seizures, muscular problems Fever, dyspnoea
45
What can convert bradyzoites to tachyzoites for rapid replication
Immunosuppression
46
What sort of issues do foetuses show in congenital toxoplasmosis when acquired tachyzoites form mother
Microcephaly, mental retardstion, visual defects
47
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
Retinal pigment epithelium
48
Why is good ifny responses of host shown to stop ocular toxoplasmosis development
Block replication by interfering with tryptophan pathway of parasites
49
Which hla allele associated with protection from ocular toxoplasmosis
Hla A29
50
Which protein from rhoptries in toxoplasma (some) associated with developing ocular toxoplasmosis and pathogenic potential
Rop16 because it downregulated rh1 responses through inducing an m2 macrophage shift (il10 is immunosuppressive)
51
How many new cases of leishmania are there every year
1 mill
52
Which arthropod vector required
sandflies
53
Which type of leishmania is most common but name all 3
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
What cell type have leishmania adapted to infect and survive/ reproduce in and what do they transition to from promastigotes injected by bite
Macrophages Turn into amastigotes which multiple in macrophages
55
Does this mean they are obligate ic
Yes
56
Which skin dysbiotic increase was shown to get worse symptoms of cutaneous leishmania major infection and five specific example of how from mice models
Staph and streptococcus Staph xylosis specifically can upregulste il17 responses leading to an inflammatory response and tissue damage (neutrophil recruitment)
57
What is a common visceral leishmania species
Donovani
58
How did this species show gut microbes of sandflies can affect outcome of infection/ cause dissemination to visceral organs in mice
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
Which virus infects and increases parhogeneitictg of leishmania
Lrv1 totiviridae
60
What does this induce which activates mirna Mir-155
Tlr3 (recognises dsrna)
61
Why is this important
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
Why was it suggested mt were acquired later in the phylogenetic tree of euk
Because early euk trichomonass and MICROSPORIDIA seemed to not have mt
63
Which apical organelle is suggested to be important for forming a parasitophorous vacuole
Rhoptries and their contents
64
Give examples of parabasalia
Trichomonas
65
Give example of diplomonads (excavata lineage)
Giardia lamblia
66
What adhesion proteins are released from micronemes for better attachment of apicomplexans
TRAP family proteins (thrombospondin related)
67
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
Tryptophan synthase b Can produce tryptophan from Indole derived from the Microbiota
68
Why would a greater level of epithelial damage be seen with cryptosporidium
Usually immunockmpetent can intercept the merozoites after release before infecting other cells
69
How is gondii commonly transmitted
Oocyst contaminated water/food Tissue cysts in uncooked meat Congenital transmission
70
Like cryptosporidium , what do toxoplasma gondii form when ic so don’t come in contact eg the merozoites in macrophages
A parasitophorous vacuole
71
What is the difference between trypanosoma brucei (gambiense and rhodensiese) and cruzi
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
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
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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