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Infection and Immunity > 25 Protozoa > Flashcards

25 Protozoa Flashcards

1
Q

how can parasites survive in the host

A

Hiding away
immune modulation
molecular mimicry
keeping one step ahead

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2
Q

how do parasites ‘hide away’

A

e.g. inside other cells or in tissues with little protection

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3
Q

how do parasites create immune modulation

A

e.g. by secretion of cytokine-like molecules

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4
Q

how do parasites create molecular mimicry

A

e.g. making coats or individual proteins look like host

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5
Q

how do parasites ‘keep one step ahead’

A

e.g. by constantly switching identity of surface proteins

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6
Q

when can parasites be transferred by insects

A

At micrometers size can start to see RBC – this small can be transmitted by flying insects e.g. mosquitos
Plasmodium falciparum are so small can get inside RBC and multiply

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7
Q

how do small, single celled parasites differ when interacting with host immune system

A
  • different survival strategies

- can do anything larger parasites cannot e.g. grow to large numbers inside a cell

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8
Q

what are protozoan parasites like

A

small (unicellular) and non-photosynthetic that isn’t a fungus (or fungus-looking)

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9
Q

what are the 2 protozoan phyla in particular important for human parasitology

A

Apicomplexa Euglenozoa (including Kinetoplastida)

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10
Q

effect of protozoan parasites on killing

A

Combined, protozoan parasites are responsible for ~1 million deaths each year, and >300 million people are at risk of being infected

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11
Q

what are the Kinetoplastid cells

A

leishmanias and trypanosomes

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12
Q

how are Kinetoplastid cells defined

A

presence of mitochondrial DNA in the kinetoplast organism

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13
Q

how do Kinetoplastid cells move

A

Has a single flagellum – swimming and motility

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14
Q

what can causes Leishmaniasis

A

more than 20 different species of the genus Leishmania

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15
Q

what leads to Leishmaniasis disease

A

following sand sly bite, incubation period from days to one year

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16
Q

how do Leishmaniasis diseases heal

A

diseases span self-healing cutaneous to a frequently fatal visceral form

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17
Q

what effects the clinical manifestations of Leishmaniasis

A

infections Leishmania species but also on host factors

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18
Q

what is cutaneous leishmaniasis

A

L. major or L. tropica

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19
Q

what is mucocutaneous leishmaniasis caused by

A

L. (Viannia) braziliensis or L. (Viannia) guyanensis

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20
Q

where does Mucocutaneous leishmaniasis infect

A

Ulcers of the skin, mouth and nose

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21
Q

where does Cutaneous leishmaniasis infect

A

skin ulcers at the site of bite (with amastigotes in it), which can heal or complicate

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22
Q

what causes Visceral leishmaniasis

A

L. chagasi

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23
Q

what does Visceral leishmaniasis cause

A

fever progressing to anemia, wasting, enlarged liver and spleen, bleeding and breathing difficulty. Death within 6-12 months

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24
Q

who gets PKDL

A

patients with visceral disease; likely to arise from persister-type parasites

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25
Q

what is the sandfly life cycle

A
  • extracellular: promastigote in the sand fly vector
  • sand fly delivers growth-arrested metacyclic promastigotes
  • intracellular amastigotes in the mammalian host
  • sand fly takes up amastigotes in bloodmeal
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26
Q

what is the mechanism of host cell invasion by Leishmania

A

Once in host
- favourite host cell is macrophage
Can overcome complement
phagocytosis – engulf body – exactly what leishmania wants

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27
Q

how does Leishmania overcome complement

A
  • Lipohosphoglycan
  • Major Surface Protease (MSP/Gp63)
  • CR3-C3bi-Gp63 and other interactions, facilitate phagocytic entry
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28
Q

how does LPG overcome complement

A

LPG prevents killing by MAC

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29
Q

how does MSP/Gp63 overcome complement

A

cleaves C3b to C3bi – inhibits MAC

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30
Q

what happens if the macrophage receptor recognises ligand

A

triggers a cascade that leads to phagocytosis – engulf body – exactly what leishmania wants

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31
Q

what do promastigotes differentiate into

A

replicative amastigotes. These tolerate low pH and are resistant to acid hydrolases (need no major modifications to phagosome to survive

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32
Q

what happens after phagocytosis

A

secreted LPS inhibits vATPase recruitment and lysosomal fusion

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33
Q

how are the sand fly infections transmitted

A

all-natural infections are initiated by the bite of the infected female sand flies

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34
Q

what does the saliva contain in a sand fly

A

vasodilators and parasite chemotactic factors

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35
Q

what do sand fly co-transmit

A

bacteria and viruses

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36
Q

what is the skin like

A

immunologically active organ

37
Q

what happens at the skin when sand fly bites

A

immune cells present or rapidly recruited

bite injury initiates wound-healing and inflammatory responses

38
Q

what does sand fly increases

A

migration of inflammatory cells to the bite site, enhancing interaction of Leishmania with host cells

39
Q

what do the neutrophils do in innate immune cells

A
  • neutrophils are first to arrive

- neutrophils are professional phagocytes – kill obligatory intracellular pathogens via ROS or NET

40
Q

Leishmania and NET

A

most Leishmania species escape NET

41
Q

what is on the Leishmania cell surface that inhibits lysosome fusion to phagosome

A

LPG and phosphatases

42
Q

what do LPG and phosphatases

A

blocking respiratory burst and superoxide anion production in neutrophils

43
Q

what do leishmania-infected neutrophils secrete

A

C-C chemokine ligand 3 (MIP-1)

C-C chemokine ligand 2

44
Q

what is the effect of the leishmania infection

A

recruitment of DC to site of infection

45
Q

what do leishmania-infected neutrophils express

A

apoptotic markers (promastigotes can delay or accelerate neutrophil apoptosis to their advantage)

46
Q

what is the effect of C-C chemokine ligand 3 (MIP-1)

A

promote phagocytosis by DC

47
Q

what is the effect of C-C chemokine ligand 2

A

recruitment of monocytes from the blood

48
Q

what do monocytes differentiate into - leishmania-infected neutrophils secrete C-C chemokine ligand 2

A

DC, migrate to lymph nodes, and promote differentiation of TH1 cells by producing IL-1

49
Q

involvement of innate immune cells - leishmania-infected neutrophils secrete C-C chemokine ligand 2

A
  • TH1 migrate to infection site

- parasite elimination via NO production and/or enhanced ROS by macrophages

50
Q

what do MO and DC engulfed promastigotes do

A

activate their TLR9 signalling and produce IL-12 (pro-inflammatory cytokine)

51
Q

what do IL-12 do

A

primes naïve T cells to Th1 response

induces NK and CD4+ and CD8+ T cells to produce of IFN-gamma (key cytokine to host protection)

52
Q

what does IFN-gamma activate

A

MO to kill intracellular parasite

53
Q

what does IFN-gamma block

A

IL-10 production (anti-inflammatory cytokine)

54
Q

what does IFN-gamma inhibit

A

expansion of CD4+ Th2 cells

55
Q

why is IL-10 important

A

regulator of immunity in leishmaniasis

56
Q

what does IL-10 do in immunity in leishmaniasis

A

protecting against leishmania causes hyper inflammation (activation of inflammasome, dead cells, pro-inflammatory cytokines etc)

57
Q

what does IL-10 down regulate

A

Th1 cells

58
Q

what does IL-10 inhibit

A

IL-2, TNF and MO activation of T cells

59
Q

what does the anti-inflammatory role of IL-10 help

A

progression and chronicity

60
Q

what can Leishmania enhance

A

disease by dampening immune response

61
Q

what are the protective and pathological anti-Leishmania immune response

A

Same cell types have been associated with either host protection or disease progression (depending on parasite species and host genetic background)

62
Q

where are monocytes and neutrophils recruited

A

monocytes and neutrophils rapidly recruited to infection site, where they clear parasites via ROS and NET

63
Q

where do DC migrate

A

migrate to lymph node where they activate and polarise T cells

64
Q

what does IFN-gamma and TNF activate

A

infected MO to kill intracellular parasites via NO

65
Q

what does TH2 and TH17 do

A

promote infection control and resolution

66
Q

what does subsequent development of IL-10 do

A

producing cells dampen the immune response, avoiding development of chronic infection

67
Q

what does excessive recruitment of monocytes cause

A

hyper-inflammation

68
Q

what does disproportionate Th17 response induces

A

tissue destruction

69
Q

what does exaggerated IFN-gamma and TNF production cause

A

tissue destruction

70
Q

what do cytotoxic granzymes and perforin by CD8+ promote

A

parasite dissemination

71
Q

what does excessive Th2 promotes

A

parasite persistence and chronic infection

72
Q

how is african trypanosomes and sleeping sickness transmitted

A

tsetse fly

73
Q

African trypanosomes - Trypanosoma brucei infect

A

many mammals, NOT humans, disease of livestock. Game animals seem able to control parasitaemia and tolerate infection with few symptoms

74
Q

African trypanosomes - what is T. b. rhodesiense indistinguishable from

A

indistinguishable from brucei except infects humans

Endemic in most east and southern African countries = Zoonosis

75
Q

what is T. b. rhodesiense

A

Acute human disease that kills in few weeks/months

76
Q

African trypanosomes - what does T. b. gambiense infect

A

mostly humans and some domestic animals. Chronic human disease that can last months/years. Endemic of most west and central African countries = specialist of humans

77
Q 
in Human African trypanosomiasis (HAT)
Early stage (stage I) where are parasites infecting
A

tissue fluids surrounding the fly bite site, enter bloodstream

78
Q 
in Human African trypanosomiasis (HAT)
Early stage (stage I) where are parasites proliferating
A

circulation in bloodstream and tissue fluids

79
Q 
in Human African trypanosomiasis (HAT)
Early stage (stage I) where are parasites causing
A
  • Fever, severe headache, muscle pain
  • As disease progresses in lymph and blood: anaemia due to autoagglutination of RBC and haemolysis cardiovascular, endocrine and kidney disorders
80
Q 
in Human African trypanosomiasis (HAT)
late stage (stage II) where are parasites infecting
A

invade central nervous system (CNS)

capillaries around the brain, from where they cross the blood-brain barrier

81
Q 
in Human African trypanosomiasis (HAT)
late stage (stage II) where are parasites causes
A
  • Invasion of the CNS and resultant inflammation
  • Sleep disturbances, alteration of mental state
  • Altered gait and reflexes, neurological and motor changes, lethargy, coma and death
82
Q

what is on the Trypanosoma brucei cell surface

A

bloodstream-form trypanosome is covered in coat of variant surface glycoprotein (VSG)

83
Q

what is VSG molecule

A

homodimer

84
Q

where is VSG molecule

A

anchored to surface by GPI (glycosyl phosphatidyl inositol)

85
Q

what clears VSG

A

Fast and focal endocytosis clears VSG-bound host AB

86
Q

what causes VSG coat change

A

Period switching of VSG coat = antigenic variation

  • periodic change in immunological ‘identity’
  • switching of VSG coat
87
Q

Antigenic variation in T. brucei - what surrounds it

A

dense coat of VSG completely enshrouds the parasite

88
Q

how is T. brucei shielded from AB

A

Invariant surface molecules

89
Q

how many antigens in antigenic variation in T.brucei are expressed at once

A

A vast repertoire of antigens to switch to/from; only 1 ever expressed at any one time

Infection and Immunity (29 decks)

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