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BIOL2022 Past Papers > Host-Parasite Part 2 > Flashcards

Host-Parasite Part 2 Flashcards

(42 cards)

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1
Q

Name one disease causes by parasite

A

Lymphatic Filariasis

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2
Q

What are the 3 parasites that Lymphatic filariasis?

A
  1. Wuchereria bancrofti -106 million cases
  2. Brugia malayi -12.5 million cases
  3. Brugia timori
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3
Q

What is filariasis caused by?

A

Nematodes

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4
Q

Parasitic disease:Filariasis

The 2 major stages in the life cycle of Wuchereria bancroft

A
  1. Human Stages
  2. Mosquito Stages
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5
Q

Larva forms in human stage

A

L3,L4,L5

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6
Q

Larva forms in Mosquito stages

A

L1-L3

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7
Q

Diagram question

Explain the life cycle of Wuchereria bancroft?

A
  1. Mosquito blood meal
    >L3 larvae enter ->lymphatics
  2. Adults in Lymphatics ) L3,L4,L5
    >Grows and mates (7-10cm) upto 7 years
  3. Female adults->sheathed microfilariae
    >migrates ->lymph and blood channels
    4.Mosquite blood meal (ingests microfilariae)
    >Microfilariae ->gut of mosquito
    >Hatches from sheath ->L1
  4. Microfilariae sheds sheaths penetrate-> mosquito’s midgut ->thoracic muscles
    6+7. L1 differentiates -> L3 Larvae
  5. L3 migrates to head and mosquito’s proboscis
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8
Q

In the W.bancroft, the mosquito is said to be?

A

Intermediate Host

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9
Q

How many months does the L3-L4-L5 process take?

A

6 months

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10
Q

Diagram question

Lympathic filariasis- Explain immune Response against Nematode (L3) using diagram

A
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11
Q

How does the L3 Larvae evade the immune system?

A
  1. Uses immune response to biting to enter bloodstream
  2. Blocks Toll-like receptors
  3. Inhibit T cell activation
  4. Promotes regulatory T cells
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12
Q

Immune evasion-Responses to Insect Bites

A
  • Biting triggers mast cell degranulation
  • > Release of histamine-> vasodilation
  • > Blood vessel wall becomes permeable to L3
  • > entry route into the bloodstream and migration towards host cell
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13
Q

Immune evasion: Block Toll-like receptors

A
  • Inteferes with TLR - Langerhan cell and dendritic cells (APCs) on skin
  • Via parasitic protiens
  • Avoids recognition
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14
Q

Immune evasion- Inhibiting T-cell Receptor (TCR)

A
  • Larvae 3- produce ES-62 protein
  • > glycoprotein attached to phospholipids
  • binds on membrane of T cell and taken in
  • > inhibits PKC signalling pathway (responsible for TCR activation)
  • T cell not activated
  • Target larvae not destroyed
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15
Q

Larvae: Promoting Regulatory T cells

A
  • Promotes T cells to differentiate ->T regulatory cells
  • Role: Immune suppression including parasites
  • How?
  • > interaction with antigen presenting cells
  • > > key role in determining fate of T cells
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16
Q

What protein is produced by L3 Larvae to inhibit TCR

A

ES-62 protein

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17
Q

How does the L3 modify the immune system?

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A
  • IL-10 :Class switching to IgG4
  • Blocks binding IgE to FceRI
  • Competes with the binding site (IgG4 binds to FecRI)
  • Results in dampened immune system
  • > Reduced IL-4
  • > Reduced IgE
  • Survival stratedy for Parasite- no mast degranulation, no complement system, no antibody dependent cell-mediated cytotoxicity (ADCC)
18
Q

Why is limiting the immune response crucial for both parasite and host cell?

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A

Parasite survival
* Strong immune system would inhibit stages in its life cycle
* >infection, reproduction and infection

Host
* Strong immune response -> tissue damage and pathology if not regulated
* >histamine -> inflammation and tissue damage

Dying worms
* Adult larvae/microfilariae
* Antigen released -> host lymphatic system
* Host recognises-> attack
* Prolonged- > damage to lympathic system + surrounding tissue
* Overtime> Fimbrotic blockage and calcification
* >impairs tissue and organ function

19
Q

What is lymphatic stone function

Study These Flashcards
A
  • Lymphatic don’t function
  • No drainage of tissue fluid
  • >Elephantiases
20
Q

What is the second micro parasitic group called?

Study These Flashcards
A

Leishmanioisis

21
Q

Leishmanioisis

Study These Flashcards
A

Protist= Trypanosome
Genus=Leishmania

22
Q

What are the 3 forms of Leishmanioisis

Study These Flashcards
A
  1. Cutaneuos
  2. Mucocutaneous
  3. Visceral
23
Q

Most common form

24
Q

Most severe form

25
Cutaneous Leishmanioisis
* Affect skin, mucous membrane * >skin sores and lesions * >localised skin lesions
26
Mucocutaneous Leishmanioisis
* Affects skin and mucous membranes * >destruction legions * >Nose, mouth and throat
27
Visceral Leishmanioisis
* Affects internal organs * >spleen,liver and bone marrow * Fatal if not treated
28
What are the 2 developmental forms of protozoan parasite of the genus Leishmania
**Amastigote** * Non-motile * Exist within host cells **Promastigote** * Motile,elongated,flagellated forms * Found in midgut of sandfly vector
29
What is kinetoplasts?
* Distinctive organelles-> amastigotes and promastigotes * specialised within mitochondria * Characterised: uniqure structure and DNA content (kDNA) * Contributes to survival and replication
30
Explain the life cycle of Leishmania
1. Sandfly blood meal (infective stage) >ingest **promastigotes** into human host cell bloodstream >Saliva of sandfly- chemotactic factor releasing agents- mediate macrophage and neutrophiles to site of infection 2. Promastigotes phagocytosed by neutrophil >within phagolysosome >evades phagocytosis destruction 3. Neutrophils short-lived- releases promastigotes. Consumed by macrophages. 4. Within macrophages- promastigotes differentiate into amastigote developmental form. (diagnostic stage) >evade phagocytosis destruction 5.Amastigotes multiple >imfects macrophage-> dies >infect other tissues and macrophages 6.Sandfly bloodmeal- picks up parasitised cells containing amastigotes 7.Amastigotes migrate from anterior midgut and differentiate back into promastigote development form 8.Sexually reproduce and migrate forwards from mid-gut to foregut. 9.Cycle repeats.
31
In the Leishmania life cycle - Which is the primary host and why?
Sandfly Sexual Reproduction occurs
32
In the Leishmania life cycle- Which is the secondary host
Humans
33
Sandfly examples
Phlebotomus – Africa, Asia, Europe  Lutzomyia- New World
34
# Modifying inflammatory pathway Sandfly biting
Injects promastigote->host bloodstream Saliva * chemotactic (brings neutrophil and macrophages to site of infection) * Blocks sandfly gut * >increase feeding behaviour * >>high change of transmission
35
# Modifying inflammatory pathway Phagocytosis by Neutrophils and Macrophages
* Prevent fusion of phagocytic vacuole with tertiary granule * >superoxide, H+ * >>lethal to parasite
36
# Modifying inflammatory pathways Persistence in Neutrophils and Apoptosis
* Harbor promastigotes in 'vacuoles' * Neutrophil- apoptosis * >delayed by parasite to persist longer
37
# Modifying inflammatory pathway Uptake of Parasites by Macrophages
* Activates complement system to be taken up my macrophages
38
# Modifying inflammatory pathways Differentiation to Amastigotes
* In macrophages- become non-motile * >to reside and multiply
39
# Modifying inflammatory pathways Parasite Spread and Multiplication
* Multiply within macrophages * Infected macrophages- transport amastigotes ->lymph nodes, sleen, liver * Multplies within these tissues >>establishing infection
40
Schematic depiction of modifying inflammatory pathway
41
Differing host immune responses leads to disease – MOUSE DATA
Black mice (protective immunity) * Leishmania infection cleared * why? * Type 1 response - activated macrophages * NO toxic to leishmania White mice (productive infection) * Infection persist * >Type 2 response * >mediate parasite growth
42
Pathology- TGFβ (cytokine- transforming growth factor beta)
* Infected macrophage * e.g Kupffer cells in liver recruit CD4 (Th2) and CD8 * >induce TGFβ and CCL (**connective tissue growth factors)** * >leadings to fibrosis- excessive formation of connective tissue * and granuloma formation- organized collections of immune cells

BIOL2022 Past Papers (10 decks)

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