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Human Molecular Parasitology > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

How many neglected disease diseases are there?

What is their budget?

A

35

$3.4

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2
Q

Which parasites are tier 1 neglected diseases?

A

Malaria

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3
Q

What tier do the kinetoplastids and helminths exist in?

A

Tier 3

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4
Q

What is the new name for neglected tropical diseases?

A

Neglected diseases of poverty

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5
Q

How many people are infected with on these Neglected diseases of poverty, 17 in total?

A

~1.4 billion

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6
Q

What percentage of registered drugs are for these diseases?

A

Less than 1%

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7
Q

What is required for the diagnosis and treatment methods for these diseases?

A

They must be cheap

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8
Q

WHat must be considered with parasite infections?

A
  • Parasite diversity
  • Parasite life cycle in host
  • Active host-pathogen interactions
  • Antigen load
  • Concomitant immunity
  • Pathology
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9
Q

Why are parasites more difficult to target with drugs?

A

They are eukaryotic - very similar to us. Therefore many drugs are poisonous and the therapeutic window is very narrow

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10
Q

What are the two groups of protozoan?

A

Apicomplexans - plasmodium
Have apical complex is involved in celluar invasion, cytoskeletal features for motility
Trypanosomatids- have a kinetoplast, have flagella for movement, no apical complex (no polar cellular invasion)

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11
Q

Why do protozoans adapt their morphology during their life cycles?

A

For survival in changing environment and as a response to stress

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12
Q

What are the three cycles of the malaria life cycle?

A

1) Sporogonic (mosquito)
2) Exo-erthrocytic (human)
3) Erythrocytic (human)

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13
Q

Outline the malaria life cycle

A
  • Mosquito takes a blood meal and injects sporozoites from saliva gland
  • Sporozoite travels to liver and infects liver hepatocyte cell
  • Liver schizont is formed; nuclear division without cellular division. No clinical symptoms
  • Schizont ruptures and enters blood stream as merozoites and infect red blood cells
  • Trophozoites mature to form schizonts which rupture to release more merozoites; clinal symptoms - cyclical fevers
  • Can differentiate into gametocytes to be taken up in a blood meal.
  • In the mosquito stomach microgametes penetrate macrogemetes to generate zygotes
  • The zygotes become motile and elongated; ookinetes
  • Ookinetes invade the midgut wall and develop into oocycts
  • Ooocysts grow and rupture to release sporozoites with travel to the salivary glands
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14
Q

Outline the human african trypanosomiasis (HAT) life cycle of T. brucei and T. rhodesiense

A
  • Tsetse fly takes blood meal and injects metacyclic trypomastigotes
  • metacyclic trypomastigotes transform into bloodstream trypomastigotes
  • trypomastigotes multiple by binary fission in various body fluids
  • trypomastigotes taken up by tsetse fly blood meal
  • trypomastigotes transform into procyclic trypomastigotes in tsetse fly midgut, which multiply by binary fission
  • procyclic trypomastigotes leave the midgut and transform into epimastigotes
  • epimastigotes multiply in salivary gland by binary fission and transform into metacyclic trypomastigotes
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15
Q

What does HAT cause?

A

Sleeping sickness due trapping in the wrong types of tissue e.g. brain

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16
Q

Outline the T. cruzi

A
  • Triatomine bug takes blood meal, and leaves faecal matter containing the parasite on the skin which is rubbed into the bite by the human
  • Metacyclic trypomastigotes penetrate various cells at the bite site, transforming into amastigotes
  • Amastigotes the multiply by binary fission in the cells of infected tissues
  • Intracellular amasitogtes transform into trypomastigotes and burst into bloodstream
  • Trypomastigotes can then infect other cells and clinical manifestations can result
  • Triatomine bug takes blood meal and ingests trypomastigote
  • Transforms into epimastigote in midgut
  • Multiply by binary fission
  • Transform into metacyclic trypomastigotes in hindgut
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17
Q

What does T. cruzi cause?

A

Chagas disease

18
Q

Outline the Leishmania spp life cycle

A
  • Sandfly takes blood meal and injects promastigote, from throat not salivary gland, into the skin
  • Promastigote is phagocytised by macrophage
  • Promagtigote transofrms into amastigote inside the macrophage
  • Amastigotes multiply in cells (including macrophages) of various tissues
  • Sandfly takes a blood meal and ingests macrophage full of amastigotes
  • Macrophage is ingested and amastigotes released
  • Amastogotes transform into promastigotes stage in mudgut
  • Promastigotes divide in midgut and migrate to proboscis
19
Q

Outline the Toxoplasma gondii life cycle

A
  • Ingested as tissue cyst or oocyte
  • Transform into tachyzoites shortly after ingestion and localise in neural and muscle tissue and develop into tissue cyst bradyzoites
20
Q

Outline the Entamoeba histolytica life cycle

A
  • Cysts and trophozoites passed in faecal matter
  • Ingestion of contaminated faecal matter
  • Trophozoites are rleased and travel to large intetsine
  • Trophozoites multiply by binary fission and produce cysts
21
Q

Outline the Giardia lambia life cycle

A

Similar to Entamoeba histolytica but contaminates water and food

22
Q

What type of transmission is shown by Entamoeba histolytica and Giardia lambia

A

Contaminative or faecal -oral transmission

23
Q

What are the three main classes of helminth parasite?

What are the important features?

A

Tapeworm: Cestodes
Flukes: Trematodes
Round worms: Nematodes
Infection by larvae or eggs, adults do not replicate, egg/larvae stages cause pathology

24
Q

What type of life cycle is seen in tapeworm?

A

Contaminative life cycle with cystic stage

25
Q

What type of life cycle is seen in Schistosoma spp?

A

Invasive life cycle
Cercariae in water penetrate in skin and circulate to the bowel, producing eggs which cause immune response and are shed to spread the parasite

26
Q

Outline the wucheria bancrofti life cycle

A
  • Mosquito takes a blood meal and L3 larvae enter the skin
  • Larvae develop into adults and commonly live in the lymphatics
  • Adults produce sheathed microfilariae which migrate in lymph and blood
  • Mosquito takes a blood meal and ingests the microfilariae
  • microfilariae shed sheaths and penetrate midgut and migrate to thoraic muscles
  • microfilariae develop into L1 larvae and then L3 larvae
  • L3 larvae migrate to proboscis
27
Q

What is interetsing about the filariael worms?

A

They have a symbiotic bacteria called Wolbachia

28
Q

Define pathology

A

A deviation form the healthy or normal state

29
Q

Define pathogenesis

A

Process based on physiological, biochemical or molecular mechanisms, and which leads to harmful effects for the host

30
Q

Define virulence

A

A reduction in host fitness as a consequence of the infection by a parasite

31
Q

What are the main categories for pathology?

A
  • Impairing capacity, mechanical interference, competition for nutrients
  • Tissue destruction
  • Virulence factors
  • Toxins
  • Proteases
  • Response exhaustion
  • Self-damaging (immunopathology)
32
Q

What are the two circulatory systems of the immune system?

How is movement achieved in each?

A

Arterial-venous, pumping by the heart, and lymphatic, hydrostatic pressure

33
Q

What roles do stromal cells play within lymphatic tissues?

A

1) Substance to the organ
2) Organised means for intra-cellular communication
3) Important environmental cues to direct immune function

34
Q

What do the architectural constraints on lymph nodes provide?

A

An increased efficiency of the immune response by promoting rare cell interactions

35
Q

How are fate decisions of lymphocytes decided?

A

By consulting with the innate immune response and other lymphocytes. The decisions can be reversible or fixed.

36
Q

Why is balance important in an immune response?

A

Enough to deal with the infection but not so much to start damaging the host tissue

37
Q

What 7 things must be remembered about the immune system?

A

1) Immune system has complex circuitry
2) Immune system has complex microarchitecture
3) Cellular components of the immune system are intimately linked
4) We have reductionist view due to in vitro work
5) Lymphocytes come in many flavours
6) Balance in response is important
7) Immune responses are dynamic and change over time

38
Q

What is type 1 hypersensitivity?

Give an example parasite that induces it

A

Extreme immune response mediated by interaction of the IgE molecule with mast cell. Cross linking of IgE molecule leads to release of granules form mast cells
e.e Filariasis

39
Q

What is type 2 hypersensitivity?

Give an example parasite that induces it

A

Extreme immune response mediated by interaction of the IgG on NK cells and antibodies on other cells
e.g. Plasmodium infected RBC

40
Q

What is type 3 hypersensitivity?

Give an example parasite that induces it

A

Extreme immune response mediated by interaction of IgG molecules with soluble antigen
e.g. Malaris

41
Q

What is type 4 hypersensitivity?

Give an example parasite that induces it

A

Extreme immune response mediated by interactions of T cells
e.g. Leishmaniasis

Human Molecular Parasitology (8 decks)

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