Immunology of infectious disease Flashcards

(36 cards)

1
Q

what are the two main tissue destruction mechanisms of extracellular bacteria?

A
  • induce inflammation

- toxins

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2
Q

what are the main immunological responders to tissue borne antigens?

A

lymph nodes

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3
Q

what compound do neutrophils release during degranulation to lower local iron concentrations?

A

lactoferrin

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4
Q

deficiencies in C5-C9 predispose to infection from what organism?

A

neisseria

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5
Q

the alternative pathway relies on what to be activated?

A

microbial surface

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6
Q

which antibody is responsible for opsonizing and enhancing phagocytosis?

A

IgG

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7
Q

which antibodies activate the classical complement pathway? what is the result?

A

IgM and IgG

lysis of bacteria

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8
Q

maternal antibodies disappear in infants after how long? what infections are infants then susceptible to?

A

3-6 months

n. meningitidis, s. pneumoniae, h. influenzae type B

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9
Q

most common immunodeficiency in the human population involves what antibody? why are they often asymptomatic?

A

IgA

IgM can compensate

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10
Q

IgA opsonize bacteria at mucosal sites via what main three mechanisms?

A
  • aggregates bacteria to facilitate expulsion
  • prevents invasion of bacteria through the mucosal epithelium
  • fixes complement
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11
Q

what component of bacteria allows them to resist phagocytosis and may inhibit complement activation via the alternative pathway?

A

polysaccharide capsule

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12
Q

forms of evasion

A
  • polysaccharide capsule
  • variation of surface antigens
  • production of IgA1 protease (neisseria, h. influenzae)
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13
Q

how does s. pyogenes interfere with complement activation?

A

produces strain-specific M proteins

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14
Q

how does s. pneumoniae interefere with complement activation?

A

produces C3 protease

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15
Q

how does s. typhi evade the immune system?

A

‘syringe’ that allows secretion of proteases across macrophage plasma membrane to inhibit the NFkB mediated signaling pathway and secretion of TNFa

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16
Q

what are the deleterious effects of the immune system, generally?

A

septic shock

superantigens

17
Q

which superantigen is responsible for toxic shock syndrome? what occurs as a result?

A

TSST-1: large release of TNFa and IL-1

18
Q

what do superantigens do?

A
  • bind to MHC II proteins on APCs and to certain Vb chains on T cells - activates T cells
  • septic shock like reaction due to T cells and macrophages producing TNFa
19
Q

what are the two most clinically relevant spirochete organisms?

A

treponema pallidum - syphilis

borrelia burgdorferi - lyme disease

20
Q

what is the main innate immune response to spirochetes?

A

neutrophils (but weak)

21
Q

what is/are the main type of immunity(ies) to combat spirochetes? what is the mechanism?

A

cell mediated (clearing) and adaptive (prevent further infection)

  • Th1 immunity most effective in CLEARING organisms
  • antibodies opsonize + protective immunity (latent syphilis)
22
Q

how does borrelia evade the immune system?

A
  • coats itself with amorphous host material - prevents phagocytosis
  • evades adaptive immunity
23
Q

what is the innate immune response to fungi?

24
Q

what type of adaptive immunity is effective against fungi?

A

humoral AND cell mediated

most importantly - cell mediated - Th1 (CTLs, granulomas)

25
what is the role of adaptive immunity in parasite infections?
- IgE production (Th2 mediated response - mast cells release histamine to increase lymph flow to flush out parasites) - Th1: CTLs, macrophages-mediated killing and/or IgG - Th2: IgE and infiltration by eosinophils
26
protozoa that survive within macrophages stimulate what type of immunity?
Th1
27
how do CD4+ T cells combat protozoa?
secrete IFNy to activate macrophages
28
what is the main immune response against plasmodium?
Th1 - CTLs against intrahepatic stage of parasite
29
what is the main evasion strategy for: african trypanosomes leishmania
trypanosomes - vary surface antigens | leishmania - suppress macrophage production of IL-12
30
what are the deleterious effects of the immune response in: cerebral malaria chronic parasite infections schistosoma eggs
- cerebral malaria - increased TNFa - chronic parasite infections - immune complexes (vasculitis and nephritis) - schistosoma eggs - liver fibrosis, portal HTN, cirrhosis
31
what specific bacterial structures are recognized by phagocytes?
RGD sequences - arginine, glycine, aspartate
32
what component of DNA activates macrophages?
unmethylated CpG dinucleotide motifs
33
how does neisseria evade the immune system?
changing surface antigens
34
what is the main method of immune evasion for t. pallidum?
- lacks virulence factors | - resistant to normal host immune mechanisms
35
immunologically, how does the lymphedema result from filarial worm infestation?
- worms lodge in channels - chronic Th1 response - severe fibrosis of lymph channels
36
how do parasites inhibit the development of Th1 immunity to vaccine antigens?
chronic infestations induce strong Th2 immunity