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Semester 3 > Infection Session 7 > Flashcards

Infection Session 7 Flashcards

1
Q

Under what circumstance does the virtually non-pathogenic coagulase -ve staphylococcus become pathogenic?

A

Upon introduction of an invasive therapy

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2
Q

Is Neisseria meningitidis strictly speaking a pathogen or commensal?

A

Commensal of the nasopharynx as it is only rarely pathogenic

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3
Q

What method of infection does strep pyogenes use to cause pharyngitis?

A

Invasion

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4
Q

What are the four methods of infection on surfaces?

A

Invasion
Migration
Inoculation
Haematogenous

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5
Q

Give some examples of external surface infections.

A 
Cellulitis
Pharyngitis
Conjunctivitis
Gastroenteritis
UTI
Pneumonia
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6
Q

Give some examples of internal surface infections.

A 
Endocarditis
Vasculitis
Septic arthritis
Osteomyelitis
Empyema
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7
Q

What prosthetic surfaces can lead to surface infections?

A 
Intravascular lines
Peritoneal dialysis catheter
Prosthetic joints
Cardiac valves
Pacing wires
Endovascular grafts
Ventriculo-peritoneal shunts
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8
Q

What is the most likely cause of prosthetic valve endocarditis

A

Coagulase -ve staphylococci from patient’s/surgeon’s skin

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9
Q

What is the pathogenesis of native valve endocarditis?

A

Bicuspid valve –> turbulent blood flow –> damaged endothelium –> platelets –> bacteria become lodged –> vegetation

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10
Q

What four process occur simultaneously in pathogenesis of infection at surfaces?

A

Adherence to host cells/prosthetic surface
Biofilm formation
Invasion and multiplication
Host response

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11
Q

Do most humans carry the same species of bacteria in the same areas as part of their microbiota?

A

Yes

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12
Q

What happens to bacterial metabolism when a biofilm is formed?

A

Decreases until only slime secretion continues

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13
Q

What induces bacteria to shrink to a spore-like state in biofilm formation?

A

Starvation

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14
Q

What turns ‘swimmers’ into ‘sinkers’ within minutes of biofilm formation starting?

A

Gene expression

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15
Q

What do bacteria that have attached to a surface do in biofilm formation?

A

Multiply and encase the colony w/a slimy matrix of mucopolysaccharides

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16
Q

What is the function of the slimy mucopolysaccharide layer in biofilm formation?

A

Aids sticking and protects against cellular and chemical defences

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17
Q

How do nutrients reach bacteria in a biofilm?

A

Diffusion into the matrix

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18
Q

What facilitates exchange of molecular signals to regulate bacterial behaviour in a biofilm?

A

Close proximity of cells

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19
Q

What relates microenvironments for different bacterial species and levels of activity within a biofilm?

A

Chemical gradients

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20
Q

What is the effect of antimicrobials on bacteria in a biofilm?

A

Damage outer cell layers but community is resistant

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21
Q

How can endocarditis lead to a brain abscess?

A

Shear forces propel aggregated cells to roll/ripple along a surface whilst remaining in protected biofilm

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22
Q

What does quorum sensing control?

A

Sporulation
Biofilm formation
Virulence factor secretion

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23
Q

How does quorum sensing control bacterial function in a biofilm?

A

Via autoinducers, cell surface/cytoplasmic receptors and gene expression

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24
Q

Why can diagnosis of causative agent in biofilm formation be difficult?

A

Adherent organisms, low metabolic state microbes or small colony variants can make culture difficult

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25
Q

What is the treatment plan for infection on a surface?

A 
Sterilise tissue
Decrease bioburden (decrease metabolic activity of biofilm)
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26
Q

How can an infection on a surface be prevented?

A

Maintain integrity of natural surfaces, prevent contamination of prosthetic surfaces and prevent/remove colonising bacteria

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27
Q

What is hypersensitivity?

A

Antigen-specific immune responses that are either inappropriate or excessive and result in harm to the host

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28
Q

What are the four types of hypersensitivity reaction?

A

I: immediate
II: antibody mediated
III: immune complex mediated
IV: cell mediated

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29
Q

How quickly does type I hypersensitivity occur in allergy prone individuals on exposure to environmental, non-infectious antigens?

A

~30 mins

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30
Q

How long does type II hypersensitivity take to occur after exposure?

A

5-12 hrs

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31
Q

What molecules are involved in type II hypersensitivity?

A

IgG or IgM

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32
Q

How is type III hypersensitivity different to type II?

A

Only takes 3-8hrs

Soluble antigens are present

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33
Q

Which cells are involved in type IV hypersensitivity?

A

T cells and macrophages

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34
Q

How long does type IV hypersensitivity take to occur after exposure?

A

24-48hrs

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35
Q

What initiates types II-IV hypersensitivity reactions?

A

Exposure to environmental infectious agents and self antigens

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36
Q

What is the normal process which prevents us from having allergies?

A

Born with TH2 phenotype
Exposure to environmental factors to educate immune system to what is safe/unsafe
Develop TH1 phenotype

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37
Q

What happens in response to stimulus when an individual has TH2 phenotype?

A

Develop increased IgE

38
Q

What factors are thought to contribute to a persistence of the TH2 phenotype leading to atopy?

A 
Small family size
Stable intestinal microflora
Good sanitation
Low or no helminth burden
Low orofaecal burden
39
Q

What factors are thought to contribute to development of a TH1 phenotype?

A 
Large family size
Rural homes (inc. interaction w/livestock)
Variable intestinal microflora
High helminth burden
High orofaecal burden
40
Q

What is the implication of clinical cross-reactivity in allergy?

A

Degree of homology between allergens due to charged proteins therefore being allergic to one substance means you are likely to be allergic to another

41
Q

It is possible to be allergic to anything?

A

Almost

42
Q

Can any allergen have the capacity to trigger a severe allergic reaction?

A

Yes

43
Q

Give two examples of clinically important allergens.

A

Medications

Latex

44
Q

What is hypersensitivity?

A

Antigen-specific immune responses that are either inappropriate or excessive and result in harm to the host

45
Q

What are the four types of hypersensitivity reaction?

A

I: immediate
II: antibody mediated
III: immune complex mediated
IV: cell mediated

46
Q

How quickly does type I hypersensitivity occur in allergy prone individuals on exposure to environmental, non-infectious antigens?

A

~30 mins

47
Q

How long does type II hypersensitivity take to occur after exposure?

A

5-12 hrs

48
Q

What molecules are involved in type II hypersensitivity?

A

IgG or IgM

49
Q

How is type III hypersensitivity different to type II?

A

Only takes 3-8hrs

Soluble antigens are present

50
Q

Which cells are involved in type IV hypersensitivity?

A

T cells and macrophages

51
Q

How long does type IV hypersensitivity take to occur after exposure?

A

24-48hrs

52
Q

What initiates types II-IV hypersensitivity reactions?

A

Exposure to environmental infectious agents and self antigens

53
Q

What is the normal process which prevents us from having allergies?

A

Born with TH2 phenotype
Exposure to environmental factors to educate immune system to what is safe/unsafe
Develop TH1 phenotype

54
Q

What happens in response to stimulus when an individual has TH2 phenotype?

A

Develop increased IgE

55
Q

What factors are thought to contribute to a persistence of the TH2 phenotype leading to atopy?

A 
Small family size
Stable intestinal microflora
Good sanitation
Low or no helminth burden
Low orofaecal burden
56
Q

What factors are thought to contribute to development of a TH1 phenotype?

A 
Large family size
Rural homes (inc. interaction w/livestock)
Variable intestinal microflora
High helminth burden
High orofaecal burden
57
Q

What is the implication of clinical cross-reactivity in allergy?

A

Degree of homology between allergens due to charged proteins therefore being allergic to one substance means you are likely to be allergic to another

58
Q

It is possible to be allergic to anything?

A

Almost

59
Q

Can any allergen have the capacity to trigger a severe allergic reaction?

A

Yes

60
Q

Give two examples of clinically important allergens.

A

Medications

Latex

61
Q

Is the sensitisation phase of allergy clinically silent or pathological?

A

Silent

62
Q

What must happen for the effector phase of allergy to be clinically pathological?

A

Re-exposure to same antigen from sensitisation phase

63
Q

What is directly activated in the first exposure to an allergen?

A

Mast cells
C3a
C5a

64
Q

What is the effect of plasma cells (B cells) on 2nd exposure to an allergen?

A

Produce antigen-specific IgE to bind to allergen

65
Q

What leads to degranulation of granular cells upon second exposure to an allergen?

A

Cross linking of allergen bound to IgE and granular cell

66
Q

What granule contents are released both in the sensitisation and effector phases of allergy?

A

Histamine
Leukotrienes
Prostaglandins

67
Q

What are the effects of granule contents release in the immune mechanism of allergic reaction?

A

Increased vascular permeability
Vasodilation
Bronchial constriction

68
Q

How can granule contents from mast cells be used in diagnosis of allergy?

A

Measure blood/serum levels to see if they are raised

69
Q

What is the result of mast cells activation in the epidermis?

A

Urticaria

70
Q

What is the effect of mast cell activation in the deep dermis?

A

Angioedema

71
Q

When does angioedema become a medical emergency?

A

When the upper respiratory airways are involved

72
Q

What are the results of systemic mast cell activation?

A 
Hypotension
CV collapse
Generalised urticaria
Generalised angioedema
Breathing problems
73
Q

What are the characteristics of S/S of anaphylaxis?

A

Sudden onset and rapid progression involving more than one organ system due to circulatory collapse

74
Q

What is the treatment for anaphylactic shock?

A

Immediate IM adrenaline

75
Q

Which receptors does adrenaline act on to reverse peripheral vasodialtion, decreases oedema and alleviate hypotension in anaphylactic shock?

A

Via alpha-1-adrenoceptors

76
Q

Which receptors does adrenaline act on to reverse airway obstruction in anaphylactic shock?

A

Via beta-2-adrenoceptors

77
Q

What is the action of adrenaline treatment on beta-1-adrenoceptors in anaphylactic shock?

A

Increase force of myocardial contraction

78
Q

What action does immediate adrenaline treatment have on mast cells in anaphylactic shock?

A

Inhibit is activation

79
Q

Will only one dose of adrenaline be required to treat anaphylactic shock and why?

A

No, likely to need further doses due to biphasic allergic response

80
Q

How are chronic allergic diseases treated?

A

With steroids to reduce immune mechanism of response

81
Q

What four methods can be used to diagnose allergy?

A

Clinical Hx
Blood tests
Skin prick tests
Challenge tests

82
Q

What features of a clinical Hx will lead to a diagnosis of allergy?

A

Atopy
Allergen
Seasonality
Route of exposure

83
Q

What is measured in blood tests looking for allergy?

A

Serum allergen-specific IgE
Serum mast cell tryptase
Serum/urinary mast cell histamine

84
Q

How is a skin prick test performed?

A

Stop antihistamine Tx 48hrs prior to test
Try to activate mast cells in epidermis –> wheal&flare >3mm=+ve
Use saline as a control

85
Q

What types of allergens are challenge tests used to investigate?

A

Food and drug

86
Q

What risks are associated with skin prick and challenge tests for allergy?

A

Anaphylaxis in highly sensitised pts

87
Q

How can allergy be managed?

A 
Avoid/eliminate allergen
Education of pt of S/S, triggers and Tx
Medic alert ID
Short/long acting drugs
Allergen desensitisation
88
Q

How do short and long acting histamines differ apart from their duration of action?

A

Short are sedating

Long are non-sedating

89
Q

What causes wheezing in allergic reaction?

A

Mast cell activation in the lung

90
Q

What is lacking when only the sensitisation phase of allergic reaction takes place?

A

IgE

Semester 3 (50 decks)

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