Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIOL2022 Past Papers > Host-Parasite Part 2 > Flashcards

Host-Parasite Part 2 Flashcards

1
Q

Name one disease causes by parasite

A

Lymphatic Filariasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is filariasis caused by?

A

Nematodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Parasitic disease:Filariasis

The 2 major stages in the life cycle of Wuchereria bancroft

A
  1. Human Stages
  2. Mosquito Stages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Larva forms in human stage

A

L3,L4,L5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Larva forms in Mosquito stages

A

L1-L3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Intermediate Host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagram question

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What protein is produced by L3 Larvae to inhibit TCR

A

ES-62 protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does the L3 modify the immune system?

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?

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

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

What is the second micro parasitic group called?

A

Leishmanioisis

21
Q

Leishmanioisis

A

Protist= Trypanosome
Genus=Leishmania

22
Q

What are the 3 forms of Leishmanioisis

A
  1. Cutaneuos
  2. Mucocutaneous
  3. Visceral
23
Q

Most common form

A

Cutaneous

24
Q

Most severe form

A

Visceral

25
Q

Cutaneous Leishmanioisis

A
  • Affect skin, mucous membrane
  • > skin sores and lesions
  • > localised skin lesions
26
Q

Mucocutaneous Leishmanioisis

A
  • Affects skin and mucous membranes
  • > destruction legions
  • > Nose, mouth and throat
27
Q

Visceral Leishmanioisis

A
  • Affects internal organs
  • > spleen,liver and bone marrow
  • Fatal if not treated
28
Q

What are the 2 developmental forms of protozoan parasite of the genus Leishmania

A

Amastigote
* Non-motile
* Exist within host cells
Promastigote
* Motile,elongated,flagellated forms
* Found in midgut of sandfly vector

29
Q

What is kinetoplasts?

A
  • Distinctive organelles-> amastigotes and promastigotes
  • specialised within mitochondria
  • Characterised: uniqure structure and DNA content (kDNA)
  • Contributes to survival and replication
30
Q

Explain the life cycle of Leishmania

A
  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
Q

In the Leishmania life cycle - Which is the primary host and why?

A

Sandfly
Sexual Reproduction occurs

32
Q

In the Leishmania life cycle- Which is the secondary host

A

Humans

33
Q

Sandfly examples

A

Phlebotomus – Africa, Asia, Europe
Lutzomyia- New World

34
Q

Modifying inflammatory pathway

Sandfly biting

A

Injects promastigote->host bloodstream
Saliva
* chemotactic (brings neutrophil and macrophages to site of infection)
* Blocks sandfly gut
* >increase feeding behaviour
*&raquo_space;high change of transmission

35
Q

Modifying inflammatory pathway

Phagocytosis by Neutrophils and Macrophages

A
  • Prevent fusion of phagocytic vacuole with tertiary granule
  • > superoxide, H+
  • > > lethal to parasite
36
Q

Modifying inflammatory pathways

Persistence in Neutrophils and Apoptosis

A
  • Harbor promastigotes in ‘vacuoles’
  • Neutrophil- apoptosis
  • > delayed by parasite to persist longer
37
Q

Modifying inflammatory pathway

Uptake of Parasites by Macrophages

A
  • Activates complement system to be taken up my macrophages
38
Q

Modifying inflammatory pathways

Differentiation to Amastigotes

A
  • In macrophages- become non-motile
  • > to reside and multiply
39
Q

Modifying inflammatory pathways

Parasite Spread and Multiplication

A
  • Multiply within macrophages
  • Infected macrophages- transport amastigotes ->lymph nodes, sleen, liver
  • Multplies within these tissues&raquo_space;establishing infection
40
Q

Schematic depiction of modifying inflammatory pathway

A
41
Q

Differing host immune responses leads to disease – MOUSE DATA

A

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
Q

Pathology- TGFβ (cytokine- transforming growth factor beta)

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions