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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
What is the treatment plan for infection on a surface?
``` Sterilise tissue Decrease bioburden (decrease metabolic activity of biofilm) ```
26
How can an infection on a surface be prevented?
Maintain integrity of natural surfaces, prevent contamination of prosthetic surfaces and prevent/remove colonising bacteria
27
What is hypersensitivity?
Antigen-specific immune responses that are either inappropriate or excessive and result in harm to the host
28
What are the four types of hypersensitivity reaction?
I: immediate II: antibody mediated III: immune complex mediated IV: cell mediated
29
How quickly does type I hypersensitivity occur in allergy prone individuals on exposure to environmental, non-infectious antigens?
~30 mins
30
How long does type II hypersensitivity take to occur after exposure?
5-12 hrs
31
What molecules are involved in type II hypersensitivity?
IgG or IgM
32
How is type III hypersensitivity different to type II?
Only takes 3-8hrs | Soluble antigens are present
33
Which cells are involved in type IV hypersensitivity?
T cells and macrophages
34
How long does type IV hypersensitivity take to occur after exposure?
24-48hrs
35
What initiates types II-IV hypersensitivity reactions?
Exposure to environmental infectious agents and self antigens
36
What is the normal process which prevents us from having allergies?
Born with TH2 phenotype Exposure to environmental factors to educate immune system to what is safe/unsafe Develop TH1 phenotype
37
What happens in response to stimulus when an individual has TH2 phenotype?
Develop increased IgE
38
What factors are thought to contribute to a persistence of the TH2 phenotype leading to atopy?
``` Small family size Stable intestinal microflora Good sanitation Low or no helminth burden Low orofaecal burden ```
39
What factors are thought to contribute to development of a TH1 phenotype?
``` Large family size Rural homes (inc. interaction w/livestock) Variable intestinal microflora High helminth burden High orofaecal burden ```
40
What is the implication of clinical cross-reactivity in allergy?
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
It is possible to be allergic to anything?
Almost
42
Can any allergen have the capacity to trigger a severe allergic reaction?
Yes
43
Give two examples of clinically important allergens.
Medications | Latex
44
What is hypersensitivity?
Antigen-specific immune responses that are either inappropriate or excessive and result in harm to the host
45
What are the four types of hypersensitivity reaction?
I: immediate II: antibody mediated III: immune complex mediated IV: cell mediated
46
How quickly does type I hypersensitivity occur in allergy prone individuals on exposure to environmental, non-infectious antigens?
~30 mins
47
How long does type II hypersensitivity take to occur after exposure?
5-12 hrs
48
What molecules are involved in type II hypersensitivity?
IgG or IgM
49
How is type III hypersensitivity different to type II?
Only takes 3-8hrs | Soluble antigens are present
50
Which cells are involved in type IV hypersensitivity?
T cells and macrophages
51
How long does type IV hypersensitivity take to occur after exposure?
24-48hrs
52
What initiates types II-IV hypersensitivity reactions?
Exposure to environmental infectious agents and self antigens
53
What is the normal process which prevents us from having allergies?
Born with TH2 phenotype Exposure to environmental factors to educate immune system to what is safe/unsafe Develop TH1 phenotype
54
What happens in response to stimulus when an individual has TH2 phenotype?
Develop increased IgE
55
What factors are thought to contribute to a persistence of the TH2 phenotype leading to atopy?
``` Small family size Stable intestinal microflora Good sanitation Low or no helminth burden Low orofaecal burden ```
56
What factors are thought to contribute to development of a TH1 phenotype?
``` Large family size Rural homes (inc. interaction w/livestock) Variable intestinal microflora High helminth burden High orofaecal burden ```
57
What is the implication of clinical cross-reactivity in allergy?
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
It is possible to be allergic to anything?
Almost
59
Can any allergen have the capacity to trigger a severe allergic reaction?
Yes
60
Give two examples of clinically important allergens.
Medications | Latex
61
Is the sensitisation phase of allergy clinically silent or pathological?
Silent
62
What must happen for the effector phase of allergy to be clinically pathological?
Re-exposure to same antigen from sensitisation phase
63
What is directly activated in the first exposure to an allergen?
Mast cells C3a C5a
64
What is the effect of plasma cells (B cells) on 2nd exposure to an allergen?
Produce antigen-specific IgE to bind to allergen
65
What leads to degranulation of granular cells upon second exposure to an allergen?
Cross linking of allergen bound to IgE and granular cell
66
What granule contents are released both in the sensitisation and effector phases of allergy?
Histamine Leukotrienes Prostaglandins
67
What are the effects of granule contents release in the immune mechanism of allergic reaction?
Increased vascular permeability Vasodilation Bronchial constriction
68
How can granule contents from mast cells be used in diagnosis of allergy?
Measure blood/serum levels to see if they are raised
69
What is the result of mast cells activation in the epidermis?
Urticaria
70
What is the effect of mast cell activation in the deep dermis?
Angioedema
71
When does angioedema become a medical emergency?
When the upper respiratory airways are involved
72
What are the results of systemic mast cell activation?
``` Hypotension CV collapse Generalised urticaria Generalised angioedema Breathing problems ```
73
What are the characteristics of S/S of anaphylaxis?
Sudden onset and rapid progression involving more than one organ system due to circulatory collapse
74
What is the treatment for anaphylactic shock?
Immediate IM adrenaline
75
Which receptors does adrenaline act on to reverse peripheral vasodialtion, decreases oedema and alleviate hypotension in anaphylactic shock?
Via alpha-1-adrenoceptors
76
Which receptors does adrenaline act on to reverse airway obstruction in anaphylactic shock?
Via beta-2-adrenoceptors
77
What is the action of adrenaline treatment on beta-1-adrenoceptors in anaphylactic shock?
Increase force of myocardial contraction
78
What action does immediate adrenaline treatment have on mast cells in anaphylactic shock?
Inhibit is activation
79
Will only one dose of adrenaline be required to treat anaphylactic shock and why?
No, likely to need further doses due to biphasic allergic response
80
How are chronic allergic diseases treated?
With steroids to reduce immune mechanism of response
81
What four methods can be used to diagnose allergy?
Clinical Hx Blood tests Skin prick tests Challenge tests
82
What features of a clinical Hx will lead to a diagnosis of allergy?
Atopy Allergen Seasonality Route of exposure
83
What is measured in blood tests looking for allergy?
Serum allergen-specific IgE Serum mast cell tryptase Serum/urinary mast cell histamine
84
How is a skin prick test performed?
Stop antihistamine Tx 48hrs prior to test Try to activate mast cells in epidermis --> wheal&flare >3mm=+ve Use saline as a control
85
What types of allergens are challenge tests used to investigate?
Food and drug
86
What risks are associated with skin prick and challenge tests for allergy?
Anaphylaxis in highly sensitised pts
87
How can allergy be managed?
``` Avoid/eliminate allergen Education of pt of S/S, triggers and Tx Medic alert ID Short/long acting drugs Allergen desensitisation ```
88
How do short and long acting histamines differ apart from their duration of action?
Short are sedating | Long are non-sedating
89
What causes wheezing in allergic reaction?
Mast cell activation in the lung
90
What is lacking when only the sensitisation phase of allergic reaction takes place?
IgE

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