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diseased > Parasitic diseases > Flashcards

Parasitic diseases Flashcards

1
Q

what are parasites?

A

organisms that live feed and can reproduce in a host organism

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2
Q

where are parasitic helminths most prevelent?

A

helminths live in warm, moist shaded soil so are endemic in tropical areas

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3
Q

why are helminth infection still so prevelent in tropical regions?

A

Neglected tropical disease-
they do not recieve funding and lack of eradication

so helminth infection remain highly prevelent

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4
Q

what are the 2 major classes of parasitic helminth infection (affect humans)

A

roundworms/nematodes e.g hookworm

flatworms e.g tapeworm, schistosoma

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5
Q

which human helminth is most clinically relevant?

A

Schistosoma infections cause the most morbidity and mortality.

this is because consequence of infection can be liver remodelling. fibrosis, megly and can result in liver failure

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6
Q

which helminth uses mosquitos as a host?

A) Schistosoma
B) Hookworm
C) Filaria
D) Ascaris

A

Filaria

they can cause lymphatic filaris as the microfilarae migrate to blood and lymph nnodes
this alters lymph flow causing swelling and disfigurement (elephantisis)

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7
Q

does filaria infection have higher or lower mortality than schistosoma infection?
Why?

A

Lower mortality but has a much greater MORBIDITY

as the elephantisis disfigures body
filaria infection and a different Filaria infection can result in river blindness

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8
Q

name 3 examples of soil transmitted helminths

A

Hookworms
whipworms
ascaris

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9
Q

how to STH establish infection?

A

they establish infection in intestine causing diarrhea, abdominal pain

can also influence cognitive function and lung emphysema

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10
Q

why are rodents useful models for helminth infection?

A

despite size difference, there is similar immune response is observed as in humans

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11
Q

why can’t other models like dogs or hamsters be used to model helminth infection?

A

these animals NATURALLY aqquire immunity to helminth whereas humans do not

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12
Q

why is there no human helminth vaccine despite some existing for cattle?

A

vaccines are tightly regulated and need to meet a ‘‘preferred product characteristic’’

so efficacy of vaccine needs to be very high and reduce worm and egg burden by 75% and no such vaccine has reached that criteria yet

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13
Q

what are some vaccine considerations?

A

need to be able to be effective

is there an antigen response

can the protein be scaled up?

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14
Q

how can we treat those already infected with helminths?

A

use antihelminthics

these are drugs targeting diffrent aspects of helminth membrane permeability

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15
Q

what is the issue with drug administeratieve programmes against helminths?

A

they are very expensive, can become easily disrupted (e.g covid19) and rural areas are often neglected from these programmes as hard to access

side effects with these anti-helminthics or drug resistance can occur to

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16
Q

how can genomics help with anti-helminth drug development?

A

able to identify mutations in those resistant to treatment and exploit that

able to target metabolism of helminth (drug)

Target the blood feeding pathway too (vaccine)

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17
Q

how does the body naturally try and rid of a helminth infection?
> later

A

a type 2 immune response is initiated
IL4,5,13 are secreted

this is a distinct signature for parasitic disease

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18
Q

how does the body naturally try and rid of helminth?
> initially?

A

level 1 immune system barriers like goblet cell hyperplasia ans mucus production as part of
‘‘weep and sweep’’

19
Q

what do cytokines produced bt Type 2- tcells do?
> specifically

A

they activate mast cell, eosinophil and basophils in innate immune response

activate smooth muscle cell to help with weep and sweep response

activate b-cell and IgE production in adaptive

20
Q

what do cytokines produced bt Type 2- tcells do?
> generally

A

amplify the type-2 immune response

21
Q

which receptor is the type 2 immune response driven by?
A IL-1B
B TNF-al
C IL-4al
D IgE

A

OPTION C

ubiquitously expressed on non-haematopoetic cells

essential for helminth expulsion

22
Q

what is a danger of IL-4alpha

Where is evidence for that?

A

despite its necessity for helminth expulsion ir can exacerbate liver fibrosis in schitosoma infected mice

23
Q

other than IL-4alpaha receptor what other Receptors can be targeted to eradicate helminths?

A

tuft cells can release IL-25 to activate innate lymphoid cells which produce type 2 cytokines independent of IL-4aR signalling

so could target IL-25 receptor to amplify this type 2 immune response

24
Q

what is the hygeine hypothesis?

A

immune systems are less exposed to organisms in childhood so experience high incidence of inflammatory disorders in later life

25
Q

how can helminths encourage cancer progression?
> generally

A

helmiths have been well documented to dampen the immune response

as cancer cells can evade the immune system this makes it more likely that tumour can develop

26
Q

what is old friends hypothesis

A

increase in inflammatory diseases results from a los of symbiotic organisms in host like helminth

27
Q

how do gut parasites influence the host?

A

they influence the gut microbiota leading to microbial dysbiosis

this includes short chain FA production which influences immune cell behavior

28
Q

how can gut parasites affect the lung?

A

their excretory secretory products can enter circulation (prevent airway circulation)

29
Q

what is one explaination as to how helminth can supress asthma airway inflammation

A

their ES actually encourage type 2 immune response

so increase in reg-t cell production

30
Q
A
31
Q

does helminth infection support tumour development?

A

conflicting literature, some evidence that helminths play a PROTECTIVE role and some suggest helminths can PROMOTE tumour progression

32
Q

what are some risk factors for colorectal cancer?

A

having inflammatory bowel disease can progress to CRC

diet high in omega 6 fatty acids

33
Q

how do omega 6 and omega 3 contribute to inflammation?

A

these PUFA must be consumed from diet

they can be metabolised to form pro-i or anti-i products like Prostoglandins

34
Q

how can one model colorectal cancer?

A

can use APC min/+ mice

or use Azoymethane with DSS to model inflammatory CRC

35
Q

what is the advantage of AOM/DSS model?

A

the tumors only develop in the colon whilst APC min/+ mice the tumours may develop elsewhere

36
Q

what role do the enzymes LOX and COX play in PUFA metabolism pathway?

A

COX actitiy can lead to prostaglandin production

LOX activity can lead to other molecule productions (depending on if they are catalysing omega 3 or omega 6 products)

37
Q

which omega product creates pro-inflame products?

A

omega-6 (found in plant oils and meats)

38
Q

what is aspirin an example of?

A

it is a COX inhibitor so used to model how blocking of prostaglandin synthessis affects tumour formation

39
Q

what is a key phenotype seen in CRC patients?

A

they have a ‘‘leaky gut’’ so intestinal membrane becomes very permeable

40
Q

what can the prostaglandin analogue be used for?
(experiementally)

A

this analogue cannot be degraded by 15-hydroxy PGDH

so its an agonist of PGE2-receptor
so can model how signalling pathway affects infection

41
Q

how can we identify prostaglandin signalling is occuring?

A

if there is beta-catenin- PHOSPORYLATION staining then that indicated the signalling pathway is occuring

42
Q

how could helminth infection drive prostaglandin signalling?

A

the excretory secretory products may include prostaglandins

or include enzymes part of the prostaglandin synthesis pathway

43
Q

what is phospholipase A2 and prostaglandin E synthase?

A

PLA2 and PGE2

they are enzymes part of the prostaglandin synthesis pathway

diseased (7 decks)

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