Protists and disease Flashcards

1
Q

Protists are

A

All eukaryotic organisms that are neither animals, nor plants, nor fungi

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2
Q

What are the challenges of living within blood?

A
  1. Innate immune response
  2. Adaptive immune response
  3. Low Iron conc
  4. How to infect next host
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3
Q

All trypanosomes have a stage in

A

Vertebrate blood

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4
Q

Structure of a typanosome (kinetoplastid)

A

Kinetoplast (like a mitochondrion)
Nucleus
Flagellum

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5
Q

Trypanosomes can infect

A

A wide variety of vertebrates

Wide variety of vectors

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6
Q

Vectors transmit

A

The parasites to the hosts

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7
Q

T. Brucei causes

A

African Sleeping Sickness

Human Trypanosomiasis

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8
Q

T. brucei is transmitted by the

A

Tstetse fly

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9
Q

T. brucei does not have

A

A free living stage

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10
Q

T. brucei hosts include

A

Livestock animals as well as humans

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11
Q

T. brucei life cycle

A
  1. Tsetse fly bites and takes up trypanosome
  2. Trypanosome multiplies in midgut and moves to salivary duct
  3. Tsetse fly transmits trypanosome during feeding through saliva
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12
Q

T. brucei disease progression stage 1

A
  1. Chancre (skin lesion forms) - parasite enters the blood

2. Intermittent fever and headache as trypanosome multiplies

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13
Q

T. brucei disease progression stage 2

A
  1. Moves to the CNS
  2. Produce toxins that disturb sleep and behaviour
  3. Seizures-coma-death
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14
Q

T. brucei disease stages

A

Chancre - Fever/Headache - CNS/Sleeping/seizures/coma/death

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15
Q

T. brucei evades the immune system by

A
Antigenic variation
(variant surface glycoprotein VSGs)
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16
Q

VSGs

A

Variant surface glycoproteins (on outer cell wall)

trypanosome changes expression of these genes and evades detection

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17
Q

Waves of fever and headache are due to

A

Antibody responses to the changing VSG coats

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18
Q

There are over 1000 VSG genes but

A

Only one is expressed at any one time

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19
Q

There are 20 VSG expression sites on telomeres (the ends of chromosomes) but

A

Only one is expressed at any one time

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20
Q

VSG gene switching is

A

Spontaneous

Occurs every 100 cell doublings

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21
Q

VSG gene switching involves

A

DNA arrangements or transcriptional regulation

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22
Q

T. cruzi causes

A

Chagas disease

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23
Q

The vector of T. cruzi is

A

Triatomine bug

24
Q

T. cruzi affects

A

8M people

25
Q

T. cruzi lifecycle

A

Feeds on infected blood
Trypanosome develops into infective form in triatomine hindgut
Infected form in faeces
Bites get itchy, infected faeces on hands
Rub eyes
Into bloodstream

26
Q

T. cruzi first infects

A

Mucous membranes

Then enter bloodstream

27
Q

T. cruzi stages of disease

A

Acute - fever (8-12 weeks)

Chronic - cardiac and intestinal lesions (10 years)

28
Q

T. cruzi survives in the cytoplasm of

A

Macrophages, heart cells, epithelial cells, muscle cells and gut cells

29
Q

Chronic infection occurs in

A

30% of infections

30
Q

T. cruzi can cause

A

Cardiac arrhythmia and mega colon

31
Q

T brucei contains

A

Kinetoplast
Invades CNS
Infective saliva
Always fatal

32
Q

T cruzi contains

A

Kinetoplast
Invades heart and gut cells
Infective faeces
Sometimes fatal

33
Q

Malaria is an

A

Apicomplexan parasite

34
Q

The Apicomplexa are

A

Unicellular and spore forming

35
Q

Hippocrates first described malaria in

A

500 BC

Agostino Salumbrino observed the bark of the cinchona tree (quinine) was effective against the fever in 1564

36
Q

The malaria parasite was discovered in

A

1880

1897 Ross discovered female mosquitos transmitted malaria

37
Q

Chloroquine was discovered in

A

1934

38
Q

Malaria deaths per year

A

1.5 million

82% deaths in children in sub saharan africa (mainly cerebral malaria, P falsiparum

39
Q

P. falsiparum life cycle

A

Sporozoites injected with saliva
Invade Kupffer cells (macrophages in liver)
Invade hepatocytes (divide asexually into schizonts)
Hepatocyte-schizont ruptures and releases merozoites into blood
Merozoites invades RBCs then turn into
Trophozoites OR Schizonts
Trophozoites eat RBC cytoplasm
Schizonts replicate asexually and then merozoites erupt and infect new RBCs
Some parasites enter a sexual cycle and form the infective micro or macrogametophytes

40
Q

Schizonts replicate

A

Asexually

Nuclear division WITHOUT cytoplasmic division - merozoites

41
Q

Plasmodium initially infects

A

Kupffer cells in liver

42
Q

Schizonts form in

A

Hepatocytes and RBCs

43
Q

Plasmodium life cycle summary

A

Sporozoites - Schizonts - Merozoites - Trophozites/Schizonts

Micro/Macrogametophytes

44
Q

Malaria is associated with regular episodes of

A

Fever

When the merozoites are released into the blood

45
Q

Advantages of living within a RBC

A

Rigid, resists shear stress

46
Q

Disadvantages of living within a RBC

A

Nutrient poor
Short cell life
Continuously exposed to liver and spleen and so immune system

47
Q

Plasmodium modifies the RBC

A

Form new channels for import and export of nutrients
Break down Hb into a.a.
Adhesive proteins on surface to avoid clearance by host (clumping and adherence to endothelium)

48
Q

PfEMP-1

A

P.f. erythrocyte membrane protein 1

Makes Knobs on surface

49
Q

Knobs induced by the parasite on the surface of RBC act as

A

Ligands

Bind to receptors on endothelium

50
Q

VAR genes encode for different

A

PfEMP-1 molecules

51
Q

There are 50 VAR genes but

A

Only one expressed at any one time

52
Q

In plasmodium there is a distinct expression site that can only

A

Accommodate a single var gene promotor

53
Q

VAR genes that are not being used are silenced in

A

Heterochromatin and promotor binding proteins

54
Q

Plasmodium parasites have a

A

Memory

Enables them to express different VAR genes at each peak of parasthemia

55
Q

Expression of one VAR gene tends to last for

A

Many cell cycles

About 1-2 years