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I&I WC1 > Parasitology > Flashcards

Parasitology Flashcards

1
Q

What determines the spread of schistosomiasis?

A

Determined by water snails that are necessary for the life cycle

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2
Q

How many people are schistosomiasis-infected? How many % are symptomatic?

A

200 million, of which 10% are symptomatic

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3
Q

What kind of parasite are schistosomes?

A

Flatworms = trematoda

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4
Q

What are the schistosoma species infective to humans? (5)

A
  1. S. mansoni
  2. S. haematobium
  3. S. japonicum
  4. S. mekongi
  5. S. intercalatum
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5
Q

What are the stages in the life cycle of schistosoma mansoni? (6)

A
  1. Eggs excreted through host stool/urine
  2. Eggs swell in hypotonic environment
  3. Miradicia hatch from eggs and find intermediate host
  4. Miracidia reproduce inside snails and are released as cercaria
  5. Cercaria travel to definite host en penetrate the skin
  6. Cercaria migrate into the bloodstream
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6
Q

Why do schistosoma eggs swell and burst in fresh water?

A

Hypotonic environment causes it to swell

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7
Q

What is the intermediate host of the miracidia of schistosoma?

A

Freshwater snails -> these are host-specific

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8
Q

How do miracidia find snails?

A

Chemotaxis

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9
Q

How do cercariae find their final host?

A

Chemotaxis

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10
Q

How do cercariae enter the skin of their host?

A

Their head structure contains proteases

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11
Q

What happens after cercariae penetrate skin?

A

They shed their outer surface and adopt a surface that is suitable to their new host

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12
Q

How long do cercariae remain within the bloodstream? Where do they travel afterwards, and why?

A

~7 days, travel to liver tissue, where males and females meet eachother

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13
Q

Where do schistosoma male-female pairs travel after finding one another? (2) Which species travels where?

A
  1. Portal vein = S. mansoni
  2. Blood vessels surrounding the urogenital tract = S. haematobium
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14
Q

Why do female schistosoma turn black in the bloodstream?

A

Due to digestion of erythrocytes for blood

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15
Q

How long can schistosomes survive in blood vessels? How do they remain there?

A

~10-15 years, attach to blood vessel wall using suckers

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16
Q

What causes pathology in schistosomiasis-infected individuals?

A

Eggs that become trapped in host tissue, causing granuloma formation -> leads to liver fibrosis & failure

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17
Q

How many % of eggs of schistoma are secreted, and how many % remain in blood vessels?

18
Q

Which kind of immune responses are usually responsible for the clearance of multicellular parasites?

A

Th2 responses

19
Q

What are the main cytokines of Th2-responses? (3)

A

IL-4, IL-5, IL-13

20
Q

Which innate cell type is involved in clearance of multicellular parasites? What is their mechanism of action?

A

Eosinophils -> binding and attack of helminth structures

21
Q

What is the role of B-cells in the clearance of multicellular parasites?

A

Produce IgE that produce mast cell degranulation, leading to contraction of smooth muscles & induction of mucus

22
Q

Why is a thicker mucosal surface advantageous in immune responses against parasites?

A

Thicker mucosal layer = harder to penetrate

23
Q

What is the result of IgE in anti-parasite responses? (2)

A
  1. Contraction of smooth muscles
  2. Induction of mucus production
24
Q

What type of immune response is initially started against schistosomiasis? What kind of response develops later?

A

Initially: Th1 response
Later: Th2 response

25
What causes the switch from a Th1 response to a Th2 response against schistosomiasis?
Induced by T2 ribonuclease secreted by eggs
26
What happens to the Th2 response during chronic schistosomiasis infection?
Intensity reduced by Treg response
27
What induces Treg responses in chronic schistosomiasis?
Unknown
28
What kind of outer structure do schistosomes have?
Tegument consisting of a syncytium, covered by at least a double membrane
29
What is the function of the double membrane on the outer surface of schistosomes? (2)
1. Prevents lysis by complement factors -> MAC is unable to penetrate multiple membranes 2. Outer membrane continuously shedded -> prevents immunological attack
30
How do schistosomes prevent immunological attack on their outer surface? (3)
1. Proteins & glycans on the outer surface are very similar to the host 2. Membrane contains structures that bind host components -> shields membrane from immune responses by mimicking the host 3. Membrane contains an unusual lipid composition that prevent immune responses
31
Why do structures on the outer surface of schistosomes determine host specificity?
They mimick host cell surface proteins, preventing immunological attack -> in another host, they surface proteins differ from the host, invoking immune responses
32
What is the composition of surface membranes of schistosomes? (3)
1. >50% cholesterol 2. Mainly saturated phospholipids 3. Rich in unusual fatty acids
33
What is the effect of the high amount of saturated phospholipids in the membrane of schistosomes? How is this compensated?
Make the membrane rigid. Compensated by high content of lyso-phospholipids
34
What are the effects that unusual phospholipids in the cell surface of schistosomes have on the host? (2)
1. Glycolipids stimulate production of IL-10, IL-6, TNF 2. Lyso-phospholipids stimulate TLR2, induce IL-10 production & induce Treg response
35
What happens to eggs when are secreted into the bloodstream? (5)
1. Thrombocytes quickly activated -> eggs bind to vessel wall 2. Endothelium overgrows eggs in blood vessel 3. After extravasation, eggs excrete protein factors that attract leukocytes 4. Leukocytes attach to eggs and degranulate, releasing proteases 5. Proteases dissolve ECM -> allows eggs to move
36
Why are eggs not damaged by proteases released by leukocytes?
Crosslinks in eggshel prevent degradation by proteases
37
Where can eggs move after ECM around them is broken down? (2) What is the result of each?
1. Towards lumen of bladder/intestine -> excreted 2. Deeper into tissue, causing granuloma formation
38
What is the average time for eggs to be excreted?
2-4 weeks
39
Why do adult schistosomes not cause clotting? (3)
1. Outer surface contains no clotting agonists and does contain clotting antagonists 2. They produce platelet inhibitors 3. They produce factors that interfere with secondary clotting
40

I&I WC1 (20 decks)

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