12 - Immunity to Parasites And Fungus (Steph) Flashcards

1
Q

protozoan parastes

A
  • unicellular, mostly intracellular
  • many motile, many free living and found in contaminated water
  • others move from arthropod vectors
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2
Q

metazoans

A

helminth worms, mostly extracellular

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3
Q

what immune response does a protozoan parasite elicit when in bloodstream, gut or interstitial fluids

A

humoral antibody responce

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4
Q

when a protozoan parasite is in its intracellular life cycle, what immune response does it elicit

A

cell-mediated immune response

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5
Q

what is malaria caused by

A

Plasmodium spp. carried by female anopheles mosquitos

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6
Q

plasmodium has what kind of life stages

A

multiple extracellular and intracellular stages of infection

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7
Q

throught the lifecycle of plasmodium, where does it move within the body

A

moves through liver/RBCs

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8
Q

what are the intracellular phases of plasmodium able to resist

A

Ab-based responses

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9
Q

how does plasmodium avoid good immune stimulation

A
  • short blood circulation time free parasite stage prevents good immune stimulation
  • Ab responses avoided by outer coat of shedding
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10
Q

T/F: Babesia bovis is multicellular

A

false

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11
Q

what clinical signs does Babesia bovis cause

A

hemolytic anemia (cattle fever, piroplasmosis)

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12
Q

how is Babesia bovis transmitted?

A

by bites from infected larval ticks (ixodes)

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13
Q

leishmaniasis is tranmitted through what?

A

sandflies

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14
Q

what kind of pathogen is leishmania

A

obligated intracellular pathogen

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15
Q

2 syndromes caused by leishmania

A
  • Localized cutaneous self-resolving lesion
  • Systemic visceral leishaniasis (fatal without treatment)
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16
Q

2 cells that leishmaniasis invade

A

neutrophils and macrophages

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17
Q

where do leishmaniasis live

A

in macrophage phagosomes

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18
Q

why does leishmaniasis cause skin inflammation

A

through tissue damage and sandfly salivary proteins

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19
Q

what response does leishmaniasis elicit

A

CD4+ and Th1response and Th1 delayed hypersensitivity (chronic exposure), INF-gamma secretion, M1like macrophages (iNOS, nitric oxide), eosinophils may promote unprotective Th2

20
Q

describe parasitic worms and a few examples

A

large, multicellular. NEMATODEs, cestodes, trematodes

21
Q

how do worms contaminate the environement

A

eggs contaminate food, water and feces

22
Q

are helminths intracellular or extracellular

A

exclusively extracellular

23
Q

how do helminths enter the host

A

through internal mucosa

24
Q

why do helminths have limited immune engagement

A

often do not replicate within host, giving few epitopes

25
Q

do helminths get phagocytozed

A

no, they are two large to get phagocytosed

26
Q

how do helminths hide from immunity

A

wrap themselves in host proteins and limit immunity

27
Q

how do helminths get expelled

A

IgE mediated mast cells and eosinophil degranulation
- release of histamines and leukotrienes that induce muscle contractions and mucus secretion (diarrhea, vomit and coughing)

28
Q

2 ways helminths get expelled

A

Ig-mediated past cell and eosinophil degranulation and Th2 type responce

29
Q

describe the Th2 type response for expelling helminths

A

IL-4 production, Th2 cell activation and IgE

30
Q

describe the effective and ineffective mechanism for expelling helminths

A

Th2 = effective: Includes IgE, mast cell degranulation, influx of eosinophils, antibody dependent cytotoxicity

Th1 = ineffective: macrophages and INF-gamma. Likely inhibited as an invasion mechanism, parasite might survive if this response is activated

31
Q

how are fungal infections aquired

A

ubiquitous

32
Q

how do fungal infections gain access to the host

A

via mucosae to extracellular spacesw

33
Q

what causes fungal infections

A

exogenous or endogenous commensal organisms that become pathogenic

34
Q

what kind of immunity controls most fungal infections

A

Innate immunity!
- physical barriers
- commensal microbiota. Antibacterial medications may result in yeast infections
- phagocytosis by neutrophils

35
Q

what is key for controlling fungal infections

A

PRRs: C-type lectin receptors sense cell wall components (B glucans, mannans, chitin),
- TLRs 2,4,9 and complement receptor 3
- Th1 response
- Adaptive immunity

36
Q

what increases susceptibility for fungal infections

A

Th2 response ??
T cell immunosuppressed patients

37
Q

Describe Neospora caninum

A
  • obligate intracellular parasite
  • affects cattle (abortions) and dogs
  • domestic dogs are the host
38
Q

describe the balance between Th1 + Th2 response for controlling neosporosis

A

Th1 responce –> INF-gamma –> control of infection but non viable pregancy because severe inflammation

Th2 response –> IL-4 and IL10 –> uncontrolled infection but viable preganancy

39
Q

what is key for killing neospora

A

TH1 INF-gamma and macrophages

40
Q

Immune response to intracellular bacteria, protozoa and viruses

A

Th1-type response

41
Q

Triggered by IL-12 by dendritic cells, macrophages and B cells

A

Th1-type response

42
Q

Induces pro-inflammatory cytokines including IFNg by T cells and NK cells

A

TH1-type responce

43
Q

An antibody-stimulating immune response elicited by helminth parasites

A

Th2-type response

44
Q

expression of IL-4 cytokines

A

Th2-type responce

45
Q

infiltration of eosinophils and mast cells and IgE production

A

Th2-type responce

46
Q
A