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BIOL2022 Past Papers > Host-Parasite Part 1 > Flashcards

Host-Parasite Part 1 Flashcards

1
Q

Define parasite

A
  • Lives in host organism
  • Benefits from depriving nutrients
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2
Q

Name 2 types of parasite

A

1. Obligate parasite
* Completely depends on host to survive- reproduction, growth and development
* Host complete life cycle

2. Faculatitive parasite
* Can live independently of a host
* But has ability to parasitize host when opportunitu arises
* Host does not need to complete life cycle

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3
Q

Groups of Parasitive organisms

Endoparasite

A

Live inside host cell

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4
Q

Endoparasite: Protist - Trypanosoma brucei (T.brucei)

A
  • microparasite
  • Relies on third organisms to aid transmission and complete life cyle
  • Vector/carrier = tsetse fly
  • > feeds on infected host (cattle, human or horses)
  • > T.brucie enters bloodstream of tsetfy
  • > rapidly mutlplies and migrates to salivary glands
  • Upon feeding again, tsetse injects the protist (saliva) into host and infects it
  • Protist undergoes different stages in life cycle
  • > correlated progress of disease
    SLEEPING SICKNESS IN HUMANS
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5
Q

What are parasitic worms called?

A

Helminths

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6
Q

Helminths are considered as?

A

Macroparasite

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7
Q

Name the 3 types of Helminths?

A
  1. Tapeworm (cestodes)
  2. Fluke (Trematodes)
  3. Roundworm (Nematodes)
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8
Q

Give example of Tapeworm and what it infects?

A
  • Long segmented body
  • Cysticerous (Pork tape worm)
  • > Young/intermediate
  • Affects brain,eyes, muscles and skin
  • Adult
  • > affects gut
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9
Q

Give example of Fluke and what it infects?

A
  • Flat leaf-like
  • Genus schistosoma
  • > blood vessel (host)
  • Fasciola
  • > liver/lung
  • > intermediate only resides in snails
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10
Q

Give example of roundworks and where it resides in host?

A
  • Elongated, cylinderical structure
  • Heatworm
  • > pulmonary artery ->dogs
  • Gives rise to cardiovascular issues
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11
Q

Define ectoparasites

A
  • parasites that live on surface/skin/outgrowth of skin

Examples
* Ticks
* Mites
* Fleas
* Lice

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12
Q

Helminths and Protozoa are what group of organisms?

A

Eukaryotes
> cellular complexity
> difficult to treat infections

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13
Q

What relationship do parasites have with their host organism?

A
  • Symbiotic relationship
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14
Q

Why go parasite generally have complex life cycles?

A
  • Have different developmental forms
  • changes in morphology > structure and form
  • challenging target for immune recognition and treatment
  • Contributes to disease progression
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15
Q

Key features of parasites

A
  • Ability to evade immune system
  • High antigen complexity and specificity to host cell
  • Limited lethaliy - does not aim to kill the host
  • > as parasite depends on host cells well being
  • > Evolved with hosts and its immune system
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16
Q

Why are parasite able to stay in host for a long time?

A
  • Evades immune system
  • Avoids immune destruction
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17
Q

What is a weak point of parasite that we can exploit?

A
  • Due to close relationship to host
  • > lost/gained metabolic pathways
  • > dependent upon host
  • Weak point we can exploit
18
Q

Mechanisms by which parasites can harm host

A
  • Direct damage
  • > feed -> tissue damage ->physical blockages
  • Host immune system induced damage
  • > inflammatory reactions
  • > release of toxic substances ->harmful to host
  • Death of parasite
  • > Inflammatory response
  • > calcificatiom/fibrosis
  • Serve as cariers
  • > virus/bacteria
  • > other parasite (mosquito and malaria)
19
Q

Ixodes ricinus

A
  • Dear tick
  • > lyme disease
  • Infection caught bite from infected tick
20
Q

Th1

A
  • Against intracellular pathogens
  • Against micro-endoparasites (protist)
  • Macrophage driven process
21
Q

Th2

A
  • Against extracellular pathogens
  • Against macro-endoparasites
  • Eosinophil-driven immune responses
22
Q

Protist infections

Trypanozoa brucei

A

Example: Trypanozoa brucei
* On its surface - lectin (sugar molecules)
* Host cells (dentritic/macropages) can reconise lectin using pattern recognition receptor (PRR)
* >Toll-like receptor (TLR)
* >Lectin receptor

> > innate response

23
Q

Possible diagram questions: Protist microparasite

Protist infections – aim activate macrophages and NK cells

A
  • Intracellular pathogen
  • > protozoan antigens
  • Binds to PRR on dendritic/macrphage cells
  • Productions of cytokines
  • Interleukin- 12 (IL-12)
  • > Drives naive Th2 to mature in to active Th2
  • > Activates Th2
  • Activates natural killer cells>Induces expression of cytokine IFN-gamma

IFN-gamma
* Pro-inflammatory response
* Drives maturation of naive Th2 alongside IL-12
* Activates resting macrophages -> active macrophages
* >mediate phagocytosis

24
Q

Possible diagram question- Protist microparasite infection

Innate response to Plasmodium falciparum

A
  • Microparasite= Plasmodium falciparum
  • Innate response to merazoite/Trophozoite (form of parasite)
  • > surface molecule= GP1
  • GP1 binds TLR2
  • > Activated TLR9
  • > binds to dsDNA (parasite)
  • Upon binding- release of cytokines
    * >IL-12 ->NK -> IFN-gamma ->activates macrophages
  • > IL-12-> act Th2

Activated macrophages
* Release of pro-inflammatory cytokines
* >IL-1
* >IL-6
* >TNF-alpha
*&raquo_space;hallmark for fever of malaria infections

25
Q

Protist infections

A
  • MHCII independent activation
  • > INNATE
  • NK cell and macrophages - main cell types

However
* Percentge of Th-1 cells- induced by IL-12
* and IFN-gamma activate protozoal specific B cells- acquired immunity
*&raquo_space;induce IgG2 and IgG3 in B cells
* (innate and adaptive meet)

26
Q

Macroendoparasitic infections

Macroendoparasitic infections mechanisms

A
  • IL-10 and TNF-alpha blocks IL-12 pathway
  • IL-4 is stimulator of type 2 T cell
27
Q

Difference between Protozoal and Helminth infections

A

Protists
* TH1 response (IFNγ)
* Inflammatory
* IL12, IFNγ
* Activated macrophage’ oxidative burst
* NK cells
* Antibody response mainly (+)
* IgG2
* IgG3

Helminths
* TH2 response (IL4)
* IL 10 and TGFβb limit acute inflammation via macrophages
* Rather Basophil and Eosinophil activation
* Antibody response mainly (++)
* IgG1 (mouse)
* IgG4 (man)
* IgE -class switch

Basophils and mast cells do have a role in inflammation

28
Q

Ig subtypes

A

Protozoa
* IgG2
* IgG3

Helminths
* IgG1
* IgG4
* IgE

29
Q

IgG subtype structures

A
30
Q

IgE Structure

A
31
Q

What is IgE?

A
  • Immunoglobulin (antibody)
  • Least abundant isotype - 0.05% in blood
  • Role: Against Helminth and Allergy
32
Q

How is immunity to Helminths mediated?

A
  • Already bound on Mast cells, Basophils and Eosinophiles
  • Binds to Helminths antigen
  • > IgE binds to surface of Helminths
  • causes aggregation of receptors> signalling pathway
  • > activates Eosinophils
33
Q

IgE and Allergy

A
  • Immune System overreacts to harmless substances: allergens
  • IgE bound to Mast cell receptor and Basophil receptor
34
Q

IgE Receptors

A
  • High affinity IgE receptor
  • > FcεRI
  • Expressed: Mast cells, Basophils
  • IL-5 induces FcεRI expression on Eosinophils
35
Q

Explain IgE activity in Mast cell, Basophil and Eosinophil?

A
  • Cross-linking and aggregation of receptors
  • Triggers intracellular signalling cascadee
  • > Degranulation of mast cells and basophils
  • > > release granules> extracellular environment
  • causes calcium increase in cells> release vacuoles degranulating
  • > Releases inflammatory mediators
  • > > Histamines
  • > > Cytokines
  • > > Chemokines

Hypersensitivity Reactions
>Allergic responses

36
Q

How is IgE regulated?

A
  • CD23 receptors
  • Low affinity lectinreceptor for IgE
  • > Binds to sugars of IgE
  • Has a second receptor = lectin
  • Surface of Eosinophils, mature B cells and macrophages
  • Regulation of IgE levels
  • Prevents degranulation
  • > influence concentration of IgE levels in blood plasma
37
Q

Explain the mechanism of degranulation using the diagram

A
  1. Helminth antigen binds to IgE bound high affinity IgE receptor
  2. Activates family of Kinases- Lyn (Src) and Syk
  3. Stimulates adaptor protein= LAT and gets phosphorylated
  4. Stimulated downstream signalling of PLCy = Phospholipase C gamma = enzyme
  5. Enzyme cleaves PIP2 ->DAG (diacylglycerol) and IP3 ( inositol trisphosphate) Important secondary messengers
  6. IP3 binds to receptors on endoplasmic reticulum
    > release intracellular Ca2+ from ER stores
  7. DAG remains associated with membrane. Along with Ca2+ leads to PKC (protein kinase C) mediated phosporylation
  8. Causes DEGRANULATION (granule exocytosis)
  9. Extracullar Ca2+ causes direct degranulation
  10. > > release of bioactive molecules contained in granules of Basophil and Eosinophil
38
Q

Eosinophils

A
  • 1% of white blood cells
  • granules IgE/FcεRI releases
  • > Eosinophil peroxidase, Ribonuclease -> cytotoxic activity
  • > Major basic protein (MBP)
  • > > cytotoxic membrane binding->destruction
  • > > induces degranulations of Mast cells and Basophils

8-12hrs (Bloodstream)
8-12days (Tissues)
>absence of stimulation
>Increase in allergic and chronic parasitic settings
Problem - will also destroy your tissues
>explains increased levels to allergy chronic reactions

39
Q

Basophil

A
  • 0.1% of WBC
  • Pre-formed mediators (from granules)
  • histamine**>vasodilation
  • serotonin >vasodilation
  • heparin> stop blot clot formations

newly formed lipid mediators:
* prostaglandin D2 >
* leukotriene C4 >
platelet-activating factor > highly vasodilatory

** newly formed cytokines**
* eosinophil chemotactic factor > stimulated degranulate
* interleukin-4 >Th2 immune > more IgE

Interleukin-4 critical cytokine in production ofIgE

Italics- cause smooth muscle constriction (not blood vessel)
>asthma

40
Q

Explain the positive feedback loop of IgE, Eosinophil and Basophil/Mast cell. Why is can it be a concern and how can IgE expression be regulated?

A
  • Parasitc antigen/allergen binds the IgE bound to FceRI (high affinity IgE receptor)
  • > degranulation: release of ribonuclease, lipase…
  • Produces Major Basic Protien (MBP) which activated basophil > degranulation> histamine, serotinin…
  • Basophil recuits IL-4 > class switching of B cells to IgE
  • Basophil produces eosinophil chemotatic factor (ECF) that brings more eosinophil site of infection
  • > > involved in this postive feedback

Control and Regulation
* CD23 - FceRII
* >low IgE affinity > binds to IgE when present in high concentrations
* Competes active site of FceRI

Why is regulation important?
* Overproduction chronic damage to tissue

BIOL2022 Past Papers (10 decks)

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