L14 Protozoa Flashcards

1
Q

what are protozoa

A

anything unicellular and non-photosynthetic that isnt a fungus

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2
Q

what is the protozoa group

A

position of root unclear

not a natural (true) evolutionary group

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3
Q

what are the 2 protozoan phyla important for human parasitology

A

apicomplexa

euglenozoa (inc kinetoplastida)

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4
Q

which protozoan phyla contains the most important parasites of man

A

apicomplexa

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5
Q

what are the apicomplexa parasites

A

plasmodium

toxoplasma

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6
Q

what is the plasmodium vertebrate host habitat

A

intracellular

erythrocyte and hepatocyte

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7
Q

what is the toxoplasma vertebrate host habitat

A

intracellular

macrophage and other cell types

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8
Q

what are the kinetoplastida parasites

A

leishmania
american trypanosomes
african trypanosomes

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9
Q

what is the leishmania vertebrate host habitat

A

intracellular

macrophage

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10
Q

what is the american trypanosomes vertebrate host habitat

A

intracellular - several cell types

and extracellular

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11
Q

what is the african trypanosomes vertebrate host habitat

A

extracellular

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12
Q

what is the mode of transmission for plasmodium

A

vector born mosquito

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13
Q

what is the mode of transmission for toxoplasma

A

ingestion of cysts

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14
Q

what is the mode of transmission for leishmania

A

vector born sandfly

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15
Q

what is the mode of transmission for american trypanosomes

A

vector born reduviid bug

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16
Q

what is the mode of transmission for african trypanosomes

A

vector born tsetse fly

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17
Q

what are the diplomonad parasites

A

giardia

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18
Q

what are the parabasalid parasites

A

trichomonas

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19
Q

what are the archamoeba parasites

A

entamoeba

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20
Q

what is the diplomonad vertebrate host habitat

A

extracellular

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21
Q

what is the parabasalid vertebrate host habitat

A

extracellular

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22
Q

what is the archamoeba vertebrate host habitat

A

extracellular

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23
Q

what is the mode of transmission for diplomonad

A

ingestion of cysts

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24
Q

what is the mode of transmission for parabasalid

A

sexual transmission

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25
Q

what is the mode of transmission for archamoeba

A

ingestion of cysts

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26
Q

what is the apicomplexan phylogeny

A

single complex group
diversified into lots of different classes
all parasites

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27
Q

what is the cell form for apicomplexa

A

polarised

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28
Q

what is the invasive lifecycle of apicomplexa like

A

specialised apical complex

polar cell with pointed end has specialised cells fro invasion

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29
Q

what is the apicoplast

A

remnant of photosynthetic past

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30
Q

how is malaria transmitted

A

by female Anopheles

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31
Q

how many plasmodium infect humans

A

5/6

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32
Q

what is the invasion cycle of mosquito like

A

3 invasion cycles: liver, RBC, potentially escape cycle when taken up by mosquito undergo sexual change (back to liver)

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33
Q

what is the decision stage in mosquito life cycle

A

re-enter replicative intra-erythrocytic cycle
OR
make gametes for transmission

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34
Q

what is the invasion cycle of cryptosporidium like

A

direct - simple
can reinvade gut cells multiple times
OR
exit - sexual cycle make eggs, taken back up again

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35
Q

how is cryptosporidium transmitted

A

contaminated water

36
Q

what does cryptosporidium cause

A
usually mild (diarrhea) 
self resolving
if are immunocompromised = chronic fatal illness
37
Q

what are the cryptosporidium that cause human disease

A

Cryptosporidium parvum
Cryptosporidium hominus
(plus C.felis, C.meleagridis, C.canis, C.muris)

38
Q

what is the invasion cycle of toxoplasma gondii

A

prey infected ingesting eggs
invasion in gut or escape and invade other parts of body
sexual cycle only in predator
part in prey and another in predator due to evolutionary pressure, parasite can find a niche to specialise into it

39
Q

which lifecycle is most like the apicomplexans ancestral one

A

cyrotosporidium or american trypanosome

40
Q

what is the definitive toxoplasma gondii host

A

cats

41
Q

what is the effect of toxoplasma gondii infection

A

prey have brains cysts alter behaviour (increasing transmission rate)

  • impaired motor performance
  • increased risk-taking
42
Q

what is the kinetoplastid cell like

A
single copy organelles
single mitochondrion 
single kinetoplast
flagellum 
glycosomes
43
Q

what makes it a kinetoplastid

A

kinetoplast

44
Q

how is american trypanosomiasis transmitted

A

hematophagous bugs from the family Reduviidae

45
Q

where is american trypanosomiasis prevalent

A

south and central america

46
Q

what is the american trypanosome lifecycle

A

simple
infect gut of bug
transmitted in faeces in form that invades humans
invades human tissue, lose flagellum, non motile
divide in cells, burst out in flagellate form, infect new cells

47
Q

what is the decision stage of the american trypanosome lifecycle

A

restart cycle
OR
become specialised form to infect and complete cycle in bug

48
Q

what is the acute phase effects of american trypanosome

A

fever
hepatosplenomegaly
10% mortality

49
Q

what are the chronic effects of american trypanosome

A

cardiomyopathy
nerve degeneration
megaesophagus
megacolon

50
Q

what is american trypanosomiasis known as

A

chagas’ disease

51
Q

what is human african trypanosomiasis known as

A

sleeping sickness

52
Q

what is the lifecycle of human african trypanosome

A

duplicate in insect gut
invasive form transmitted in bite
forms in blood to divide or form a form that it primed for transmission

53
Q

how does human african trypanosome move

A

highly motile

54
Q

what is the lifecycle of leishmania

A

divide in gut
migrate to saliva gland
inject to human host
division in human host and gets into other cells – intracellular

55
Q

what are the leishmania manifestations

A

cutaneous
mucocutaneous
visceral or kala-azar

56
Q

what causes cutaneous leishmania

A

L. major & L. tropica

57
Q

what is cutaneous leishmania

A

skin ulcers at the site of bite, with varied number of amastigote forms in it

58
Q

what causes mucocutaneous leishmania

A

L. braziliensis & L. mexicana

59
Q

what is mucocutaneous leishmania

A

ulcers of the skin, mouth and nose

60
Q

where does mucocutaneous leishmania occur

A

South and Central America up to Texas, US

61
Q

what causes visceral leishmania

A

L. donovani

62
Q

what does visceral leshimania cause

A
fever
anaemia
enlarged liver and spleen
bleeding 
breathing difficulty
63
Q

what is the survival of visceral leishmania

A

6-12 months

64
Q

bite site for leishmania transmission - following stages of invasion

A

saliva contains vasodilators
sand fly co-transmits bacteria and viruses
bite damages tissue, triggers neutrophil recruitment
saliva increases migration of inflammatory cells, enhancing interaction of leishmania with host cells

65
Q

leishmania mechanism of host cell invasion

A

use cell surface molecules and secretory to stimulate engulfment
need to prevent phagolysosome developing too far down lysosomal pathway and killing it – lesihmainia modify the phagolysosome behavior so it provides them with nutrients and doesn’t kill them
they grow and burst out to infect

66
Q

how does leishmania actively invade

A

no active invasion machinery

67
Q

how does leishmania survive intracellularly

A

intracellular amastigotes tolerate low pH and are resistant to hydrolases
inhibition of fusion with late endosomes
interfere with host-cell signalling

68
Q

effect of leishmania on phagosome

A

no major modification

69
Q

how does plasmodium change RBC

A

modifies RBC surface it infects – individual knobs made by parasite deliberately
made by parasite secretion PfEMP1 (for P. falciparum)

70
Q

what does PfEMP1 do

A

‘rosetting’ of erythrocytes

71
Q

how does PfEMP1 do its function

A

binds to Duffy antigen

72
Q

what is the role of the spleen

A

filters blood
removes senescent erythrocytes
metabolises haemoglobin and recycles iron

73
Q

where is the late stage plasmodium infected RBCs detected

A

in the spleen

74
Q

how does the parasite avoid spleen removal

A

rosetting – protects certain amount of the RBC surface, when goes through spleen not as obvious = reduced detection
cytoadherence (clumping) prevents parasites traveling through spleen

75
Q

what is PfEMP1 important for

A

immunity and disease

76
Q

what is the PfEMP1 gene like

A

conserved intracellular C-terminal tail

diverse extracellular region

77
Q

how do PfEMP1 vary

A

extracellular parts differ considerably = different binding properties and different recognition by immune system

78
Q

what is seen in endemic areas of plasmodium falciparum infection

A

exposure to parasite very early in life
early exposure results in most deaths and greatest disease
= either develop resistance or die

79
Q

what is acquired immunity

A

depends on antibody-antigen interaction

80
Q

what is antigenic variation

A

a system employed by various pathogens to evade acquired immunity
constantly change surface that they expose to immune system so can live extracellularly in blood system

81
Q

why is antigenic variation important

A

stands in the way of vaccination

82
Q

what is the trypanosoma brucei cell like in the bloodstream

A

covered in a coat of variant surface glycoprotein (VSG)

83
Q

why is VSG immunogenic

A

10 million copies form a monolayer

periodic change in immunological identity - switching VSG coat

84
Q

how do protozoan parasites ‘specialise’ in immune evasion

A
  1. hide away
    - intracellular
    - cytoadherence/sequestration (plasmodium)
  2. antigenic variation (plasmdoium, giardia, trypanosoma brucei)
85
Q

which are the intracellular protozoan parasites

A

apicomplexa
trypanosoma cruzi
leishmania spp.