Protists and disease Flashcards

(55 cards)

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

25
T. cruzi lifecycle
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
T. cruzi first infects
Mucous membranes | Then enter bloodstream
27
T. cruzi stages of disease
Acute - fever (8-12 weeks) | Chronic - cardiac and intestinal lesions (10 years)
28
T. cruzi survives in the cytoplasm of
Macrophages, heart cells, epithelial cells, muscle cells and gut cells
29
Chronic infection occurs in
30% of infections
30
T. cruzi can cause
Cardiac arrhythmia and mega colon
31
T brucei contains
Kinetoplast Invades CNS Infective saliva Always fatal
32
T cruzi contains
Kinetoplast Invades heart and gut cells Infective faeces Sometimes fatal
33
Malaria is an
Apicomplexan parasite
34
The Apicomplexa are
Unicellular and spore forming
35
Hippocrates first described malaria in
500 BC | Agostino Salumbrino observed the bark of the cinchona tree (quinine) was effective against the fever in 1564
36
The malaria parasite was discovered in
1880 | 1897 Ross discovered female mosquitos transmitted malaria
37
Chloroquine was discovered in
1934
38
Malaria deaths per year
1.5 million | 82% deaths in children in sub saharan africa (mainly cerebral malaria, P falsiparum
39
P. falsiparum life cycle
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
Schizonts replicate
Asexually | Nuclear division WITHOUT cytoplasmic division - merozoites
41
Plasmodium initially infects
Kupffer cells in liver
42
Schizonts form in
Hepatocytes and RBCs
43
Plasmodium life cycle summary
Sporozoites - Schizonts - Merozoites - Trophozites/Schizonts | Micro/Macrogametophytes
44
Malaria is associated with regular episodes of
Fever | When the merozoites are released into the blood
45
Advantages of living within a RBC
Rigid, resists shear stress
46
Disadvantages of living within a RBC
Nutrient poor Short cell life Continuously exposed to liver and spleen and so immune system
47
Plasmodium modifies the RBC
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
PfEMP-1
P.f. erythrocyte membrane protein 1 | Makes Knobs on surface
49
Knobs induced by the parasite on the surface of RBC act as
Ligands | Bind to receptors on endothelium
50
VAR genes encode for different
PfEMP-1 molecules
51
There are 50 VAR genes but
Only one expressed at any one time
52
In plasmodium there is a distinct expression site that can only
Accommodate a single var gene promotor
53
VAR genes that are not being used are silenced in
Heterochromatin and promotor binding proteins
54
Plasmodium parasites have a
Memory | Enables them to express different VAR genes at each peak of parasthemia
55
Expression of one VAR gene tends to last for
Many cell cycles | About 1-2 years