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Infectious Disease > Immunology of infectious disease > Flashcards

Immunology of infectious disease Flashcards

1
Q

What are the bacteria that multiply outside of the host cell?

A
  • Staph
  • Strep
  • E.coli
  • Clostridium
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2
Q

What are the two means that extracellular bacteria cause cell damage?

A
  • Induction of inflammation

- Toxins that kill the host cells

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3
Q

How does the cell combat extracellular bacterial?

A

Kill them or neutralize the toxins

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4
Q

What are the cells that can do phagocytosis? Where are each generally found?

A

PMNs–bloodstream

Macrophages–tissues

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5
Q

How does phagocytosis identify bacteria?

A

Recognize bacterial structures (e.g. polysaccharides, peptides)

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6
Q

What is the first cell that arrives to the site of inflammation?

A

PMNs

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7
Q

What is the receptor for LPS?

A

TLR4

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8
Q

What is the peptide sequence that phagocytes recognize on bacteria?

A

RGD (arg, Gly, Aspartate)

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9
Q

What are the main immunological responders to tissue borne antigens?

A

Lymphocytes

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10
Q

Where in the lymphatic system do phagocytic cells reside?

A

Lymph nodes

Spleen

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11
Q

Bacterial DNA contains what motif that can activate macrophages?

A

Unmethylated CpG dinucleotide

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12
Q

What are the receptors on phagocytic cells that can respond to bacteria?

A 
Fc receptors
Complement receptors
Scavenger receptors
Lectins
TLRs
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13
Q

What type of bacteria is complement especially important for?

A

Those with polysaccharide capsule

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14
Q

What cells release lactoferrin? What is the MOA of this?

A

PMNs

Lower local Fe concentrations to combat bacteria

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15
Q

What is the role of histamine in immunity?

A

Enhances inflammatory process by upregulating proteins on endothelial cells to aid in extravasation

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16
Q

What is the classical pathway?

A

IgG or IgM binds to bacteria, causing C1 to bind to Fc region, and activating the Attack complex

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17
Q

What is the alternative pathway of complement pathway?

A

Spontaneously hydrolysis of C3b will attach to bacteria to form the attack complex (C5-9)

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18
Q

Deficiencies in C5-C9 predisposed to what infections? Why?

A

Neisseria meningitidis infections

Neisseria for some reason needs all complements

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19
Q

What is the role of C5-C9 (in terms of gram positive and negatives)?

A

Lyses gram negative bacteria (can pop holes since lacks peptidoglycan layer)

Opsonizes gram positive

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20
Q

What is the main adaptive immune response to extracellular bacteria?

A

Humoral response (IgG)

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21
Q

What is the role of antibodies in extracellular bacterial infection ?

A
  • Enhances opsonization
  • Neutralize toxins
  • Activate complement
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22
Q

What are the two types of antibodies that activate complement?

A

IgG and IgM

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23
Q

What is the only class of Ab that can cross the placenta?

A

IgG

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24
Q

How long does it take for maternal IgG levels to disappear in the neonate? What three specific infections are the

A

3-6 months

  • Strep pneumoniae
  • Neisseria meningitidis
  • HiB
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25
Q

What is the longest lived ab? How long does this last?

A

IgG

3 weeks

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26
Q

What is the protein on S. Pyogenes and S. Pneumoniae that is a target for ab? What is the function of this?

A

M protein

Antigenic variation b/t species

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27
Q

Does IgA fix complement?

A

Yes

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28
Q

What antibody can take the place of IgA in selective IgA deficiency?

A

IgM

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29
Q

What cytokine is the most potent activator of macrophages?

A

IFN-gamma

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30
Q

What are IgA antibodies secreted with?

A

J chain

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31
Q

What is the role of the polysaccharide capsules on bacteria?

A

Resist phagocytosis, and may inhibit complement activation

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32
Q

What are the bacteria that can vary their surface antigen?

A
  • Neisseria
  • E.coli
  • HiB
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33
Q

What are the bacteria that produce IgA-1 proteases?

A
  • S. Pneumoniae
  • Neisseria
  • Hib
34
Q

How does S. pyogenes interfere with complement activation? S. pneumoniae?

A 
Pyogenes = M proteins
Pneumoniae = C3 protease
35
Q

How does S. Typhi cause avoid immunity? What does this do?

A

Type III secretion system

-syringe that allows secretion of proteases across macrophages plasma membrane to inhibit the NF-kappa-B and TNF-alpha

36
Q

What is the most common bacterial cause of septic shock? Why?

A

Gram negatives d/t LPS induces release of TNF-alpha and IL-1

37
Q

What is the MOA of superantigens?

A

Bind to class II MHC molecules on APCs, and to certain Vbeta on T cells, to cause overactivation of T cells

38
Q

What causes the septic shock with superantigens?

A

Release of TNF-alpha

39
Q

What is the superantigen that Staph Aureus releases?

A

TSST-1

40
Q

What is rheumatic fever?

A

Strep infx causes abs that are cross reactive to sarcolemma of the heart

41
Q

What is poststreptococcal glomerulonephritis?

A

Infx with strep causes immune complex formation and deposition

42
Q

What are the three major Spirochetes?

A
  • T Pallidum
  • B burgdorferi
  • Leptospirosis
43
Q

How does infection with spirochetes occur?

A

Enter through breaks in the skin or via arthropod vectors

44
Q

What type of tick transmits Lyme disease?

A

Ixodes tick

45
Q

What is the role of innate immunity with spirochetes?

A

Phagocytosis + killing
Complement cascade
but not very effective

46
Q

What is the role of adaptive immunity with spirochetes?

A

Strong cell mediated and humoral immunity

47
Q

What is the role of Th1 cells? What is the cytokine that activates this?

A

Cell mediated

IL-12

48
Q

What is the role of Th2 cells? What is the cytokine that activates this?

A

Humoral

IL-4

49
Q

What is the role of antibodies in syphilis infx?

A

Prevent reinfection

50
Q

True or false: T. pallidum elicits a strong cell mediated and humoral response

A

True

51
Q

Why is T. Pallidum tough to get rid of?

A
  • Lack virulence factors

- Resistant to normal host immune

52
Q

How does B. Burgdorferi evade the immune system?

A

Coats itself with amorphous host material to prevent phagocytosis

53
Q

What is the cause of secondary syphilis?

A
  • Immune complex deposition in the skin

- Ab that cross react with host fibronectin and collagen

54
Q

What is the cause of Lyme arthritis?

A

T cell mediated response to B. Burgdorferi

55
Q

Where in the body can fungi live?

A
  • Extracellular tissues

- Inside phagocytic cells

56
Q

What are the immune responses to fungi?

A

Cell mediated, but also humoral

57
Q

What is the major cell involved in the innate immune response to fungi?

A

PMNs

58
Q

Neutropenic individuals are particularly susceptible to what infections?

A

Fungi (candida albicans)

59
Q

Germ tube test = ?

A

Candida albicans

60
Q

What is the dominant protective mechanism against disseminated candidiasis?

A

PMNs

61
Q

What is the cell type that eliminates Cryptococcus neoformans?

A

CTLs

62
Q

What is the response to Histoplasmosis?

A

granulomas

63
Q

What is the one fungi that is particularly susceptible to abs?

A

Candida

64
Q

What are the cells that mediate a granuloma?

A

Th1 cells
Macrophages
Giant cells

65
Q

What cytokine maintains a granuloma? What cells release this?

A

IFN-gamma

Th1 cells

66
Q

How effective is the innate immunity with parasitic infections? Why?

A

Not very

Resistant to complement, and granule contents of PMNs

67
Q

What is the role of histamine in the lymp?

A

Increases lymph flow and flushes antigens into lymph nodes

68
Q

Why is it that there is generally only a Th1 or Th2 response?

A

Development of one inhibits the development of the other

69
Q

What are the parasites that survive within macrophages? What type of immune response does this elicit? How?

A

Leishmania and trypanosoma cruzi

Th1 response, via CD4 cells releasing IFN-gamma

70
Q

How does IFN-gamma aid in parasitized non-macrophages cells?

A

Depleting intracellular tryptophan

71
Q

Why is it that CTLs cannot really kill parasites in RBCs?

A

RBCs lack MHC class I

72
Q

What is the role of IgE in parasitic infections?

A

ADCC

73
Q

What are the labs that are elevated in most worm infections?

A

Eosinophilia and IgE

74
Q

What are the strategies of evading the immune system for parasites?

A
  • Conceals in cyst
  • Coast with host proteins
  • Inhibit complement activation
  • Enzymes that cleaves bound antibodies
75
Q

How does African trypanosomes evade the immune system?

A

Vary surface antigens

76
Q

How does Leishmania evade the immune system?

A

Suppresses production of IL-12 and Th1 cells, since IFN-gamma is activated by macrophages

77
Q

What is the mechanism of the deleterious effect of the immune system?

A

Dysregulated Th1 may cause cerebral malaria, for example

78
Q

What is the major deleterious immune response in chronic parasitic infestations

A

Immune complex depositions (vasculitis + nephritis)

79
Q

What is the MOA of the deleterious immune response to Schistosomiasis?

A

Severe liver fibrosis from disruption of venous flow and granuloma formation

80
Q

How does filariasis mediate a deleterious immune response?

A

Lodge in lymph channels, causing Th1 chronic fibrosis

Infectious Disease (18 decks)

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