Immunology of infectious disease Flashcards

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?

A

neutrophils

24
Q

what type of adaptive immunity is effective against fungi?

A

humoral AND cell mediated

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

25
Q

what is the role of adaptive immunity in parasite infections?

A
  • 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
Q

protozoa that survive within macrophages stimulate what type of immunity?

A

Th1

27
Q

how do CD4+ T cells combat protozoa?

A

secrete IFNy to activate macrophages

28
Q

what is the main immune response against plasmodium?

A

Th1 - CTLs against intrahepatic stage of parasite

29
Q

what is the main evasion strategy for:

african trypanosomes
leishmania

A

trypanosomes - vary surface antigens

leishmania - suppress macrophage production of IL-12

30
Q

what are the deleterious effects of the immune response in:

cerebral malaria
chronic parasite infections
schistosoma eggs

A
  • cerebral malaria - increased TNFa
  • chronic parasite infections - immune complexes (vasculitis and nephritis)
  • schistosoma eggs - liver fibrosis, portal HTN, cirrhosis
31
Q

what specific bacterial structures are recognized by phagocytes?

A

RGD sequences - arginine, glycine, aspartate

32
Q

what component of DNA activates macrophages?

A

unmethylated CpG dinucleotide motifs

33
Q

how does neisseria evade the immune system?

A

changing surface antigens

34
Q

what is the main method of immune evasion for t. pallidum?

A
  • lacks virulence factors

- resistant to normal host immune mechanisms

35
Q

immunologically, how does the lymphedema result from filarial worm infestation?

A
  • worms lodge in channels
  • chronic Th1 response
  • severe fibrosis of lymph channels
36
Q

how do parasites inhibit the development of Th1 immunity to vaccine antigens?

A

chronic infestations induce strong Th2 immunity